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| EKG changes, lethargy, torsades, confusion, seizures, coma |
hypomagnesemia |
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storeysl2 Sun, 12 Feb 2012 18:58:22 GMT |
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| tissue hypoxia, muscle weakness, paralysis, death, seizures |
hypophosphatemia |
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storeysl2 Sun, 12 Feb 2012 18:58:22 GMT |
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| tetany, lethargy, confusion, seizures |
hypocalcemia |
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storeysl2 Sun, 12 Feb 2012 18:58:22 GMT |
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| Normal levels of phosphate |
2.5-4.6 mg/dL |
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storeysl2 Sun, 12 Feb 2012 17:31:07 GMT |
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| Normal levels of Magnesium |
1.8-2.4 mg/dL |
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storeysl2 Sun, 12 Feb 2012 17:31:07 GMT |
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| How does Vitamin D affect calcium absorption? |
Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone |
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storeysl2 Sun, 12 Feb 2012 17:31:07 GMT |
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| What are good sources of calcium? |
milk, cheese, yogurt, broccoli and spinach |
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storeysl2 Sun, 12 Feb 2012 17:24:47 GMT |
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| What are good sources of Vitamin D? |
Sunlight and oily fish and nuts. |
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storeysl2 Sun, 12 Feb 2012 17:24:47 GMT |
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| What is calcium absorbed in? Mostly excreted by? And what regulates it? |
Absorbed in the small intestine. Excreted by the kidneys. Parathyroid hormone regulates calcium release from bone. |
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storeysl2 Sun, 12 Feb 2012 17:24:47 GMT |
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| Normal calcium level |
8.4-10.2 mg/dL |
1 |
storeysl2 Sun, 12 Feb 2012 17:29:27 GMT |
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| What demographic is most likely to have SLE? |
African American female |
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storeysl2 Fri, 10 Feb 2012 02:45:15 GMT |
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| What are the primary cells stimulated in Type I reactions? |
mast cells |
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storeysl2 Fri, 10 Feb 2012 02:45:15 GMT |
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| What type of hypersensitivity does NOT involve antibodies? |
Type IV |
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storeysl2 Fri, 10 Feb 2012 02:45:15 GMT |
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| Phagocytic Deficiencies |
-phagocytes are there but they cant kill whats ingested
-severe pneumonias, skin granulomas, bone infections |
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storeysl2 Fri, 10 Feb 2012 02:42:58 GMT |
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-increased neisseria infections
-C3 deficiency (most severe, shows early)
-Recurrent infections (respiratory H. influenza, S. pneumonia-encapsulated bacteria) |
Complement deficiencies |
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storeysl2 Fri, 10 Feb 2012 02:42:58 GMT |
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| Combined T and B cell deficiencies |
-severe combined immunodeficiency (SCID)
-treatment:typically a bone marrow transplant |
0 |
storeysl2 Fri, 10 Feb 2012 02:42:58 GMT |
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- Ab production is often diminished
-at risk for recurrent, life-threatening viral and fungal infections
-Chronic Mucocutaneous Candidiasis
-DiGeorge Syndrome |
T Lymphocyte Deficiencies |
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storeysl2 Fri, 10 Feb 2012 02:42:58 GMT |
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-T cell response is not typically affected
-characterized by low levels of circulating antibody
-Bruton agammaglobulinemia
-Selective IgA deficiency |
B Lymphocyte Deficiencies |
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storeysl2 Fri, 10 Feb 2012 02:39:27 GMT |
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| Secondary (acquired) immune deficiencies |
-caused by another illness
-more common |
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storeysl2 Fri, 10 Feb 2012 02:39:27 GMT |
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| Primary (congenital) immune deficiency |
genetic anomaly -sporadic mutation before birth
-Include: T cell (viral), B cell (encapsulated bacteria), Combined (everything), Complement (encapsulated), Phagocytic (encapsulated) |
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storeysl2 Fri, 10 Feb 2012 02:39:27 GMT |
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| Infections are not normal when... |
-development of unusual or recurrent, severe infections
-typical infections include: pneumonia, otitis media, sinusitis, bronchitis, septicemia, meningitis, infection with opportunist pathogens
-prolonged Abx use not effective
-suspect an immune deficiency... |
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storeysl2 Fri, 10 Feb 2012 02:39:27 GMT |
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-Immunoglobulin (polyclonal)
-decreases the number and activity of T cells
-prevent acute rejection of renal transplants
-aplastic anemia |
Lymphocyte immune globulin (Atgam)/Antithymocyte (equine) |
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storeysl2 Fri, 10 Feb 2012 02:31:07 GMT |
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-monoclonal antibodies
-blocks activation of T cells by Il2
-prophylaxis of acute organ rejection |
Basiliximab and daclizumab |
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storeysl2 Fri, 10 Feb 2012 02:31:07 GMT |
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-monoclonal antibodies
-blocks all T-cell function by binding CD3
-prevents acute rejection of transplants
-depletes T cell prior to bone marrow transplant |
Muromonab-CD3 |
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storeysl2 Fri, 10 Feb 2012 02:31:07 GMT |
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-suppress immune responses by killing lymphocytes undergoing proliferation, these drugs injure ALL proliferation cells
-Examples: Azathiprine, Methotrexate, Cyclophosphamide, except Mycophenolate which selectively inhibits B/T cell proliferation
-Adverse effects: bone marrow suppression, Gi issues, reduced fertility, alopecia
-due to toxic effects, usually reserved for pts not responding to other immunosuppressants |
Cytotoxic drugs |
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storeysl2 Fri, 10 Feb 2012 02:31:07 GMT |
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Action: suppress Ag processing via IL1 suppression, suppress proliferation of lymphocytes be suppressing IL2 production, inhibit synthesis of mast cell products, suppress phagocyte infiltration
-Use: widely suppress immune response
-Contra: vaccines & fungal infections
-Adrenal suppression: withdrawal syndrome, always taper!
-large doses used to prevent rejection
-Adverse reactions: cushingoid syndrome, increased risk for infection, impaired growth in children |
Glucocorticoids |
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storeysl2 Fri, 10 Feb 2012 02:25:09 GMT |
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-most effective immunosuppressants available
-main use:prevention of organ rejection
-typically used with glucocorticoids
-Examples: cyclosporine, tacrolimus
-Action: suppresses IL2 productions which is key for T and B cell proliferation
-Adverse effects: nephrotoxicity, infection, hirsutism, HTN, tremor
-Many drug interactions, avoid NSAIDs, avoid grapefruit juice
-Monitor drug levels! |
Calcineurin Inhibitors |
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storeysl2 Fri, 10 Feb 2012 02:25:09 GMT |
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-prevention of organ rejection
-treatment of autoimmune disease |
immunosuppressants |
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storeysl2 Fri, 10 Feb 2012 02:25:09 GMT |
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-late response (60-100 days post transplant)
-T cells in graft attack host
-immunocompromised at risk, generally not a problem if patient is immunocompetent
-Type IV hypersensitivity |
Graft-Versus-Host Disease (GVHD) |
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storeysl2 Fri, 10 Feb 2012 02:15:22 GMT |
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| What are the different transplant rejections? |
1. Hyperacute: immediate to 24 hrs, preexisting antibody, Type II hypersensitivity
2. Acute: days to months, Type IV hypersensitivity
3. Chronic: months to years, Type IV hypersensitivity |
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storeysl2 Fri, 10 Feb 2012 02:15:22 GMT |
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| What are transplantations based on? |
Getting the best possible match of human leukocyte antigens (HLA) |
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storeysl2 Fri, 10 Feb 2012 02:15:22 GMT |
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| Explain the Rh incompatibility problem. |
Rh- woman with an Rh+ fetus, cells from Rh+ fetus enter woman's bloodstream, woman becomes sensitized-antibodies form to fight Rh+ blood cells, in the next Rh+ pregnancy maternal antibodies attack fetal red blood cells, give Rhogam to suppress response to Rh+ RBCs |
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storeysl2 Fri, 10 Feb 2012 01:10:33 GMT |
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| What are some signs and symptoms of a blood transfusion reaction? |
Signs: vital sign changes, hyperkalemia from RBC lysis, urine changes
Symptoms: fever, chills, nausea, impending doom, pain, itching, dyspnea, etc. |
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storeysl2 Fri, 10 Feb 2012 01:10:33 GMT |
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| What are the two hemolytic (immune) blood transfusion reactions? |
1. agglutination
2. complement-mediated lysis (Type II hypersensitivity)
(other reactions include non-hemolytic febrile and anaphylactic, as well as issues with massive replacement) |
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storeysl2 Fri, 10 Feb 2012 00:57:34 GMT |
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| Blood Type AB |
Type A and B antigens
neither antibody |
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storeysl2 Fri, 10 Feb 2012 00:54:21 GMT |
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| Blood Type O |
No antigens
anti A and B antibody |
0 |
storeysl2 Fri, 10 Feb 2012 00:54:21 GMT |
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| Blood Type B |
Type B antigen
anti A antibody |
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storeysl2 Fri, 10 Feb 2012 00:54:21 GMT |
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| Blood Type A |
Type A antigen
anti B atnibody |
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storeysl2 Fri, 10 Feb 2012 00:54:21 GMT |
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| immune system reacts with antigens on the tissue of other genetically dissimilar members of the same species |
alloimmunity |
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storeysl2 Fri, 10 Feb 2012 00:51:33 GMT |
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| SLE drug that binds BLyS thus reducing B cell proliferations and reduces Abs. Although, it weakens the immune system. |
belimumab (Benlysta) |
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storeysl2 Fri, 10 Feb 2012 00:50:50 GMT |
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| What are some pharmcological options for SLE? |
-NSAIDs
-Corticosteroids
-Immunosuppressants |
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storeysl2 Fri, 10 Feb 2012 00:50:50 GMT |
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| What are some clinical manifestations of SLE? |
-Athralgias or arthritis
-vasculitis and ras
-renal disease
-hemtologic changes
-cardiovascular disease |
0 |
storeysl2 Fri, 10 Feb 2012 00:50:50 GMT |
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| What are some common findings in SLE (four required for diagnosis)? |
Facial rash (malar rash)
Discoid rash
Photosensitivity
Oral or nasopharyngeal ulcers
Nonerosive arthritis (2 joints)
Serositis
Renal disorder
Neurologic disorder
Hematologic disorders
Immunologic disorders
Presence of antinuclear antibodies (ANA) |
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storeysl2 Fri, 10 Feb 2012 00:50:50 GMT |
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-most common, complex, and serious of the autoimmune disorders
-chronic, multisystem inflammatory disease
-production of autoantibodies
against particularly nucleic acids
-has both Type II and III hypersensitivity mechanisms (Type II-destruction of RBCs, Type III-development of immune complexes that deposit in tissue)
-disease of flares and remissions |
Systemic Lupus Erythematosus (SLE) |
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storeysl2 Fri, 10 Feb 2012 00:45:40 GMT |
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| body recognizes self-antigens as foreign |
autoimmunity |
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storeysl2 Fri, 10 Feb 2012 00:45:40 GMT |
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| How does the TB Skin Test work? |
-protein (Ag) from mycobacterium tuberculosis is injected
-macrophages take up Ag
-if there are memory T cells to the TB Ag, they will infiltrate the area
-cause swelling
-onset is delayed |
0 |
storeysl2 Fri, 10 Feb 2012 00:42:10 GMT |
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| What are some examples of Type IV hypersensitivities? |
graft rejection, contact allergic reactions, autoimmune disease (rheumatoid arthritis, Type I DM), tuberculin skin test |
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storeysl2 Fri, 10 Feb 2012 00:42:10 GMT |
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-mediated by T lymphocytes, does not involve antibodies
-cytotoxic T cells, direct killing
-Th1 cells secrete IFNy which activates macrophages (they release lysosomal enzymes and reactive oxygen species, induce apoptosis) |
Type IV Hypersensitivity (Cell-Mediated) |
0 |
storeysl2 Fri, 10 Feb 2012 00:42:10 GMT |
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| What are some examples of Type II Hypersensitivity? |
Thrombocytopenia purpura, graves disease, hemolytic anemia |
0 |
storeysl2 Fri, 10 Feb 2012 00:42:10 GMT |
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| What are some examples of Type III Hypersensitivity? |
Serum sickness, Raynaud's, Arthus reaction |
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storeysl2 Fri, 10 Feb 2012 00:37:28 GMT |
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| What is the difference b/w Type II and Type III hypersensitivity? |
The only difference is the Ag/Ab complex forms THEN deposits in the tissue in Type III. In Type II Ab binds to Ag on the tissue. |
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storeysl2 Fri, 10 Feb 2012 00:37:28 GMT |
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-Ab binds to soluble (free) Ag forming
-Ag/Ab complexes are formed in the circulation and are later deposited in vessel walls or extravascular tissues
-not organ specific
-neutrophils try to ingest Ag/Ab complex but it is attached to tissues and thus releases toxins that destroy healthy tissue |
Type III Hypersensitivity (Immune Complex) |
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storeysl2 Fri, 10 Feb 2012 00:37:28 GMT |
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-begins with AB binding to a tissue specific Ag or an Ag that has attached to a particular tissue
-destroys cell by MAC, phagocytosis, neutrophil toxins, natural killer cell cytotoxicity
-causes target cell malfunction |
Type II Hypersensitivity (tissue) |
0 |
storeysl2 Fri, 10 Feb 2012 00:37:28 GMT |
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| What are some examples of second generation antihistamines (H1 antagonists)? |
-fexofenadine (Allegra)
-Cetirizine (Zyrtec)
-Loratadine (Claritin)
-Desloratadine (Clarinex) |
0 |
storeysl2 Thu, 09 Feb 2012 19:04:33 GMT |
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| What is an example of a first generation antihistamine (H1 antagonist)? |
diphenhydramine (Benadryl) |
0 |
storeysl2 Thu, 09 Feb 2012 19:02:53 GMT |
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| What are antihistamines contraindicated in? |
0during third trimester of pregnancy
-nursing mothers
-newborn infants |
0 |
storeysl2 Thu, 09 Feb 2012 19:02:53 GMT |
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| Antihistamines mechanism of action |
-blocks the actions of histamine by selectively binding H1 receptors
-do not block H2 receptors
-do not block histamine release
-some bind to muscarinic receptors |
0 |
storeysl2 Thu, 09 Feb 2012 19:02:53 GMT |
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| What are antihistamines used for? |
-mild allergy
-insomnia
-common cold |
0 |
storeysl2 Thu, 09 Feb 2012 19:02:53 GMT |
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| What are H2 receptor antagonists used for? |
Peptic ulcer disease |
0 |
storeysl2 Thu, 09 Feb 2012 18:54:14 GMT |
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| second generation H1 receptor antagonists |
non-sedating, do not cross BBB |
0 |
storeysl2 Thu, 09 Feb 2012 18:54:14 GMT |
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| first generation H1 receptor antagonists |
sedating, cross BBB |
0 |
storeysl2 Thu, 09 Feb 2012 18:54:14 GMT |
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| What do you use for treatment of anaphylaxis? |
epinephrine! NOT antihistamines |
0 |
storeysl2 Thu, 09 Feb 2012 18:54:14 GMT |
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| What are some later effects of histamine? |
attracts neutrophils, attracts eosinophils |
0 |
storeysl2 Thu, 09 Feb 2012 18:43:21 GMT |
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| What are some initial effects of histamine? |
bronchoconstriction, edema, vasodilation, vomiting, diarrhea, abdominal pain |
0 |
storeysl2 Thu, 09 Feb 2012 18:43:20 GMT |
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| How does Type I hypersensitivity work? |
First exposure: Ag leads to IgE production, IgE specifically binds to mast cells Fc receptor
Second exposure: Ag crosslinks the IgE bound Fc, leads to mast cell degranulation, release of histamine |
0 |
storeysl2 Thu, 09 Feb 2012 18:43:20 GMT |
|
-IgE and mast cell (histamine) mediated
-antigens that cause this allergic reaction, called allergens
-hypersensitive responses against environmental (exogenous) antigens i.e. skin, respiratory, GI |
Type I Hypersensitivity |
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storeysl2 Thu, 09 Feb 2012 18:43:20 GMT |
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| What are the four different types of hypersensitivity reactions? |
Type I: IgE-mediated
Type II: Tissue-specific reactions
Type III: Immune complex-mediated
Type IV: Cell-mediated (does not involve antibody) |
0 |
storeysl2 Thu, 09 Feb 2012 16:15:18 GMT |
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| hypersensitivity reactions that take several hours to develop, maximum severity is days after re-exposure to antigen |
delayed hypersensitivity reactions |
0 |
storeysl2 Thu, 09 Feb 2012 16:15:18 GMT |
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| hypersensitivity reactions that occur within minutes to a few hours after Ag exposure, anaphylaxis (systemic and cutaneous) |
immediate hypersensitivity reactions |
0 |
storeysl2 Thu, 09 Feb 2012 16:15:18 GMT |
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| hypersensitivity to tissue of another individual |
alloimmunity |
0 |
storeysl2 Thu, 09 Feb 2012 16:12:00 GMT |
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| hypersensitivity to self |
autoimmunity |
0 |
storeysl2 Thu, 09 Feb 2012 16:12:00 GMT |
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| hypersensitivity to the environment |
allergy |
0 |
storeysl2 Thu, 09 Feb 2012 16:12:00 GMT |
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| altered immunologic response to an antigen that results in disease or damage to the host |
hypersensitivity |
0 |
storeysl2 Thu, 09 Feb 2012 16:12:00 GMT |
|
Therapeutic uses: gram +, serious drug resistant infections, Abx associated psuedomembranous colitis (C.Diff), for patients with PCN allergy
Contra: renal impairment
Adverse effects: ototoxicity, "red man syndrome" histamine, thrombophlebitis, thrombocytopenia
TARGET: BACTERIAL CELL WALL |
Vancomycin |
0 |
storeysl2 Thu, 09 Feb 2012 16:10:09 GMT |
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| Describe MRSA |
-hospital acquired going down, community acquired going up
-staph is normally found on the skin
-can develop into MRSA cellulitis
-isolation precautions!
-drain area, send off cultures, IV Vanc, oral Abx, decolonization |
0 |
storeysl2 Thu, 09 Feb 2012 16:10:09 GMT |
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| How can antibiotics cause resistance? |
Exposure to ABx creates selection pressures:
-broad-spectrum skill other bacteria in the environment that would normally secrete toxins, overgrowth of normal flora providing conjugation potential
-not fully rigid, leaving behind bacteria
-nosocomial - environment
-use in livestock, ingested by us |
0 |
storeysl2 Thu, 09 Feb 2012 16:10:08 GMT |
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| What do bacteria do to become more resistant? |
-reduce drug concentration
-inactivate drug via enzymes
-change antigenic targets
-spontaneous mutation
-conjugate with other bacteria |
0 |
storeysl2 Thu, 09 Feb 2012 16:10:08 GMT |
|
Therapeutic uses: UTI, combination more powerful
Contra: pregnant women, nursing mothers, infants under 2 months
Adverse effects: hypersensitivity (Stevens-Johnson syndrome), photosensitivity, hematologic - hemolytic anemias, renal - crystalluria
TARGET: BACTERIAL METABOLITES (FOLIC ACID) |
Sulfanomides & Trimethoprim |
0 |
storeysl2 Thu, 09 Feb 2012 16:03:07 GMT |
|
Therapeutic uses: broad-spectrum, wide variety, not good for staph or anaerobes, inhalation anthrax
Contra: IV avoided in children due to risk of tendon rupture
Adverse effects: risk for tendon rupture- disrupts cartilage matrix, phototoxicity, absorption can be reduced by cationic solutions
TARGET: BACTERIAL DNA/RNA |
Fluoroquinolones (Cipro) |
0 |
storeysl2 Thu, 09 Feb 2012 16:03:07 GMT |
|
Therapeutic uses: narrow spectrum, serious infections, aerobic gram - bacilli
Contra: inactivates PCN do not administer together
Adverse effects: nephrotoxicity, ototoxicity, neuromuscular blockade - respiratory depression
TARGET: BACTERIAL PROTEIN SYNTHESIS - BACTERIOCIDAL |
Aminoglycosides |
0 |
storeysl2 Thu, 09 Feb 2012 16:03:07 GMT |
|
Therapeutic uses: substitute in PCN allergy
Contra: avoid admin with CYP3A4 inhibitors (increase risk of QT)
Adverse effects: GI effects, QT prolongation
TARGET: BACTERIAL PROTEIN SYNTHESIS - BACTERIOSTATIC |
Macrolides |
0 |
storeysl2 Thu, 09 Feb 2012 16:03:07 GMT |
|
Therapeutic uses: acne, periodontal disease
Contra: pregnant women, children under 8
Adverse effects: hepatotoxicity, nephrotoxicity, photosensitivity, discolor teeth, GI irritation
TARGET: BACTERIAL PROTEIN SYNTHESIS - BACTERIOSTATIC |
Tetracyclines |
0 |
storeysl2 Thu, 09 Feb 2012 15:56:36 GMT |
|
Therapeutic uses: gram -, multiple generations
Contraindications: severe PCN allergy
Adverse effects: bleeding, thrombophlebitis, abx-associated psudeomembrancous colitis, alcohol intolerance
TARGET: BACTERIAL CELL WALL |
Cephalosporins (Ceph) |
0 |
storeysl2 Thu, 09 Feb 2012 15:56:36 GMT |
|
Therapeutic uses: gram -, broad and narrow spectrum
Contraindications: renal dysfunction, severe allergy
Adverse effects: allergy, electrolyte imbalances
TARGET: BACTERIAL CELL WALL |
Penicillins (PCN) |
0 |
storeysl2 Thu, 09 Feb 2012 15:56:36 GMT |
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| What are some things that antibiotics target that make them more selectively toxic? |
-bacterial cell wall, protein synthesis, DNA/RNA, enzymes |
0 |
storeysl2 Thu, 09 Feb 2012 15:56:36 GMT |
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| ability to injure the pathogen without harming healthy cells |
selective toxicity |
0 |
storeysl2 Thu, 09 Feb 2012 15:51:25 GMT |
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| Why is it important for patients to complete the entire course of antibiotic treatment? |
failure to promotes resistance |
0 |
storeysl2 Thu, 09 Feb 2012 15:51:24 GMT |
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| any agent, natural or synthetic that has the ability to kill or suppress microorganisms |
antimicrobial drug |
0 |
storeysl2 Thu, 09 Feb 2012 15:51:24 GMT |
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| chemical produced by microbe that can harm another microbe |
antibiotic |
0 |
storeysl2 Thu, 09 Feb 2012 15:51:24 GMT |
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| When a person is FIRST exposed to most antigens, about how long does it take before an antibody can be detected in the blood? |
6 days |
0 |
storeysl2 Wed, 08 Feb 2012 16:19:56 GMT |
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| Which antibody is the first antibody produced in a typical primary immune response? |
IgM |
0 |
storeysl2 Wed, 08 Feb 2012 16:19:56 GMT |
|
| What is the function of edema in aiding in the inflammatory process? |
dilution of toxins |
0 |
storeysl2 Wed, 08 Feb 2012 16:14:57 GMT |
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| primarily produce endotoxins |
viruses |
0 |
storeysl2 Wed, 08 Feb 2012 16:14:57 GMT |
|
| What is the hallmark of most infections? |
fever |
0 |
storeysl2 Wed, 08 Feb 2012 16:14:57 GMT |
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| plasma protein system that forms a fibrinous mesh to trap proteins, phagocytic cells and microbes |
coagulation system |
0 |
storeysl2 Wed, 08 Feb 2012 16:13:38 GMT |
|
| What makes fungi so difficult to treat? |
-polysaccharide wall leads to ABX resistance
- intracellular comparison is similar to host cell |
0 |
storeysl2 Wed, 08 Feb 2012 16:13:38 GMT |
|
| How do viruses harm cells? |
Impair: stop DNA/RNA/protein synthesis, fuse host cells
Cell Lysis: disrupt lysosomal membranes releasing digestive enzymes
Impair-change: cell identity (antigens) -target for immune system, transform to cancer
Promote secondary bacterial infection |
0 |
storeysl2 Wed, 08 Feb 2012 16:13:38 GMT |
|
| How does the virus infect the host cell? |
1. absorption
2. penetration
3. uncoating
4. replication
5. assembly
6. release |
0 |
storeysl2 Wed, 08 Feb 2012 16:13:38 GMT |
|
-dependent on the host cells
-two general types, RNA and DNA |
viruses |
0 |
storeysl2 Wed, 08 Feb 2012 16:09:47 GMT |
|
| What happens when bacteria secrete endotoxins when they lyse or are growing? |
-pyrogenic, initiates inflammation, anaphylaztoxins, capillary permeability, vasodilation, cytokine release, and ultimately shock (septicemia) |
0 |
storeysl2 Wed, 08 Feb 2012 16:09:47 GMT |
|
| What happens when bacteria secrete exotoxins during growth? |
-damage cell membranes, inhibit protein synthesis, immunogenic |
0 |
storeysl2 Wed, 08 Feb 2012 16:09:47 GMT |
|
-prokaryocytes
-classified by O2 metabolism, shape, and staining |
bacteria |
0 |
storeysl2 Wed, 08 Feb 2012 16:09:47 GMT |
|
| What are some viral evasion techniques? |
-hiding within the host cells
-latency
-change antigens (antigenic shift-more gradual mutations or antigenic shift-major shifts in genetic recombination usually in species jumping) |
0 |
storeysl2 Wed, 08 Feb 2012 16:06:39 GMT |
|
| What are some bacterial evasion techniques? |
-coating to evade phagocytes
-suppress complement
-toxins to kill neutrophils
-fast proliferation
-change antigens |
0 |
storeysl2 Wed, 08 Feb 2012 16:06:39 GMT |
|
| What are the different types of unhealthy relationships with microorganisms? |
Opportunism: normal flora outside of normal environment, immunocompromised, pathogens gone wild
Pathogenicity: harms human, benefits microorganism |
0 |
storeysl2 Wed, 08 Feb 2012 16:06:39 GMT |
|
| What are the different types of healthy relationships with microorganisms? |
Symbiosis: benefit to human, no harm to bacteria
Mutualism: benefit both
Commensalism: no harm to human, benefit bacteria |
0 |
storeysl2 Wed, 08 Feb 2012 16:06:39 GMT |
|
| How do Helper T cells (Th) - Cd4+ cells work? |
1. antigen signal via MHC II binds to TCR and Cd4+
2. second cytokine signal (IL1)
3. Proliferation signal (IL2)
4-5. additional cytokine signals from the environment decides Th phenotype
6. Tc immunity (Th1) favored if IL12, IFNy
7. BC immunity (Th2) favored if IL4
8. cytokines from the proliferated Th cells can also inhibit proliferation of the other type, hence more of self develops |
0 |
storeysl2 Wed, 08 Feb 2012 16:02:52 GMT |
|
| How does the cytotoxic (Tc) cells - CD8+ kill virally infected cells? |
apoptotic mechanisms |
0 |
storeysl2 Wed, 08 Feb 2012 16:02:52 GMT |
|
| Explain cytotoxic T cell clonal selection. |
1. APC present Antigen via MHC I which binds with TCR/CD8
2. Cytokine (IL2) signal from Th1 cells induce proliferation
3. thus resulting in clones of antigen0specific effector (Tc) cells that target virally infected or cancerous cells |
0 |
storeysl2 Wed, 08 Feb 2012 16:02:52 GMT |
|
| What are T cells? |
-lymphocytes
-develop in the thymus
-cannot see antigen unless in the context of MHC and binds with the TCR |
0 |
storeysl2 Wed, 08 Feb 2012 15:57:25 GMT |
|
| Explain B cell clonal selection. |
1. antigen uptake via BCR and processed
2. Antigen presented via MHC II to Th
3. binds to TCR
4. Th releases cytokines to help proliferation of B cell
5. B cell differentiates
6. becomes antibody producing plasma cell |
0 |
storeysl2 Wed, 08 Feb 2012 15:57:25 GMT |
|
| What happens when other environmental allergens besides parasites induce IgE? |
allergies |
0 |
storeysl2 Wed, 08 Feb 2012 15:57:25 GMT |
|
| What releases eosinophils? |
mast cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:57:25 GMT |
|
| What is the only thing that can kill parasites? |
eosinophils |
0 |
storeysl2 Wed, 08 Feb 2012 15:54:05 GMT |
|
| What antibody binds to parasites? |
IgE |
0 |
storeysl2 Wed, 08 Feb 2012 15:54:05 GMT |
|
| largest antibody, earliest produced in infection and in neonate |
IgM |
0 |
storeysl2 Wed, 08 Feb 2012 15:54:05 GMT |
|
| most abundant/protective antibody, maternal antibody is major class found in fetus |
IgG |
0 |
storeysl2 Wed, 08 Feb 2012 15:54:05 GMT |
|
| Where is IgA found? |
secretions and breast milk |
0 |
storeysl2 Wed, 08 Feb 2012 15:51:52 GMT |
|
| How do antibodies protect? |
Direct: neutralization, block pathogen receptor that is required for infection of host cells, bind to toxins
Indirect: activate innate system, complement-classic pathway, macrophage binding through Fc receptor |
0 |
storeysl2 Wed, 08 Feb 2012 15:51:52 GMT |
|
| What is the structure of an antibody? |
one Fc chain that recognizes immune cells and two Fab cells that bind to antigens |
0 |
storeysl2 Wed, 08 Feb 2012 15:51:52 GMT |
|
| What do memory B cells do? |
mount quicker response following secondary exposure of antigen |
0 |
storeysl2 Wed, 08 Feb 2012 15:51:52 GMT |
|
| What do plasma B cells do? |
produce antibodies |
0 |
storeysl2 Wed, 08 Feb 2012 15:48:33 GMT |
|
| What are B cells? |
-lymphocytes
-develop in the bone marrow
-recognize antigen via B cell receptor (BCR) |
0 |
storeysl2 Wed, 08 Feb 2012 15:48:33 GMT |
|
-does not involve the individual's immune response
-rather Ab or cells are transferred from someone else (fetus, immunotherapy)
-short-lived |
Passive acquired immunity |
0 |
storeysl2 Wed, 08 Feb 2012 15:48:33 GMT |
|
-requires the individual's immune response
-by individual after natural exposure (or vaccine)
-long-lived (due to memory) |
Active acquired immunity |
0 |
storeysl2 Wed, 08 Feb 2012 15:48:33 GMT |
|
| What is cellular immunity? |
-cytotoxic (direct killing), T cell directed, aided by Th1 cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:46:26 GMT |
|
| What is humoral immunity? |
-antibody-mediated, B cell directed, aided by Th2 cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:46:26 GMT |
|
| What are two types of adaptive immunity? |
humoral immunity and cellular immunity |
0 |
storeysl2 Wed, 08 Feb 2012 15:46:26 GMT |
|
| Name examples of T cells. |
Cytotoxic T cell (Tc), Helper T cell (Th), and Memory T cell |
0 |
storeysl2 Wed, 08 Feb 2012 15:46:26 GMT |
|
| Name examples of B cells |
plasma B cell and memory B cell |
0 |
storeysl2 Wed, 08 Feb 2012 15:44:37 GMT |
|
| What is clonal selection? |
- APCs will present antigen via MHC to the unique B/T cells in the secondary lymphoid tissue
-then the one unique B/T cell that recognizes the antigen presented by the APC will multiply and build an army of antigen-specific clones |
0 |
storeysl2 Wed, 08 Feb 2012 15:44:37 GMT |
|
| What is clonal diversity? |
-during fetal development, we produce millions of B and T cells that specifically recognize ONE antigen
-they are now immunocompetent
-they then migrate to the secondary lymphoid tissue where they wait for clonal selection |
0 |
storeysl2 Wed, 08 Feb 2012 15:44:36 GMT |
|
| Where are B and T cells after birth? |
lymph nodes, spleen, Peyer's patches, tonsills/adenoids |
0 |
storeysl2 Wed, 08 Feb 2012 15:44:36 GMT |
|
| Where are B and T cells before birth? |
T cells in the thymus and B cells in the bone marrow |
0 |
storeysl2 Wed, 08 Feb 2012 15:41:02 GMT |
|
| What are the cells of adaptive immunity? |
B lymphocytes and T lymphocytes |
0 |
storeysl2 Wed, 08 Feb 2012 15:41:02 GMT |
|
| What do CD markers do? |
Biologic function: helpt to hold the communication, provides extra signals to elicit intracellular signaling processes
Diagnostic function: used in identification of immune cells by flow cytometry or for basic science experiments |
0 |
storeysl2 Wed, 08 Feb 2012 15:41:02 GMT |
|
| antigen that helps us recognize ourselves |
human leukocyte antigen (HLA) |
0 |
storeysl2 Wed, 08 Feb 2012 15:41:02 GMT |
|
| MHC II |
- on B cells, APC, and some epithelial cells, dendritic cells, and macrophages
-presents "exogenous" antigens from digested extracellular pathogens
- think bacteria
-react with CD4 on Th cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:38:07 GMT |
|
| MHC I |
-located on all nucleated cells and platelets
- presents "endogenous" antigens from intracellular proteins
- think viruses
-reacts with CD8 on Tc cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:38:07 GMT |
|
| What do antigens require? |
-processing (translation) by APCs
-presentation by APCs to Te cells in the context of MHC |
0 |
storeysl2 Wed, 08 Feb 2012 15:38:07 GMT |
|
| What do Antigen presenting cells (APCs) do? |
The reside at points of entry, such as your airway. If they find something, they take it in, eat it, and decide whether or not they should tell the T cell about it. |
0 |
storeysl2 Wed, 08 Feb 2012 15:38:06 GMT |
|
-regulate mast cells vasuclar mediators through enzyme (histaminase) that degrade histamine
-defense against parasites
-mildly phagocytic, recruited by mast cells |
eosinophils |
0 |
storeysl2 Wed, 08 Feb 2012 15:17:02 GMT |
|
| Recognize and eliminate cells infected with viruses and some function in eliminating cancer cells. Cytotoxic lymphocyte of innate system. |
Natural killer cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:17:02 GMT |
|
| How do mast cells maintain homeostasis? |
They send out more H1 in the beginning and then more H2 at the end. |
0 |
storeysl2 Wed, 08 Feb 2012 15:17:02 GMT |
|
| What does H2 do? |
-causes secretion of gastric acid
-decreases lymphocyte and eosinophil activity
-decreases chemotaxis of neutrophils
-decreases degranulation of mast cells |
0 |
storeysl2 Wed, 08 Feb 2012 15:14:38 GMT |
|
| What does H1 do? |
-contraction of smooth muscle
-contraction of endothelial cells
-increased chemotaxis of neutrophils
-prostaglandin synthesis in the mast cell |
0 |
storeysl2 Wed, 08 Feb 2012 15:14:38 GMT |
|
| What do mast cells synthesize? |
-prostaglandins, platelet activating factor, and leukotrienes |
0 |
storeysl2 Wed, 08 Feb 2012 15:14:38 GMT |
|
| What do mast cells release when degranulation occurs? |
histamine and chemokins |
0 |
storeysl2 Wed, 08 Feb 2012 15:14:38 GMT |
|
| What are the two ways mast cells release their contents? |
1. degranulation
2. synthesis of lipid-derived chemical mediators |
0 |
storeysl2 Wed, 08 Feb 2012 15:10:36 GMT |
|
| What activates mast cells? |
physical injury, chemical agent, immunologic processes, toll-like receptors, anaphylatoxin |
0 |
storeysl2 Wed, 08 Feb 2012 15:10:36 GMT |
|
| What are mast cells? |
cellular bags of granules located in loose connective tissues close to blood vessels. |
1 |
storeysl2 Wed, 08 Feb 2012 15:11:01 GMT |
|
| What is the central cell in inflammation? |
mast cells! |
0 |
storeysl2 Wed, 08 Feb 2012 15:08:39 GMT |
|
| What can a1-antityrpsin deficiency lead to? |
COPD |
0 |
storeysl2 Wed, 08 Feb 2012 15:08:39 GMT |
|
| What does a1-antityrpsin do? |
It neutralizes enzymes to protect surrounding cells from lysosozymes, proteases, etc. |
0 |
storeysl2 Wed, 08 Feb 2012 15:08:39 GMT |
|
| What does phagocytic death result in? |
Rupture of the cell and release of contents. |
0 |
storeysl2 Wed, 08 Feb 2012 15:07:00 GMT |
|
| Do superoxides only destroy bad tissue? |
No! They destroy good tissue to. THis is why antioxidnats are important so that they can clean up all the superoxide. |
0 |
storeysl2 Wed, 08 Feb 2012 15:07:00 GMT |
|
| What do oxygen-independent phagolysozomes do? |
-acidic pH 3.5-5
-defensin/cathelicidins-attack membrane
-enzymatic attack - proteases, myeloperoxidase, etc.
-inhibition of growth by lacteoferrin binding iron |
0 |
storeysl2 Wed, 08 Feb 2012 15:07:00 GMT |
|
| What do oxygen-dependent phagolysosomes do? |
-alteration in glucose transport
-generation of reactive oxygen species (free radicals)
-superoxide - hydrogen peroxide
-directly kill microbes |
0 |
storeysl2 Wed, 08 Feb 2012 15:07:00 GMT |
|
| How do phagocytes get to the pathogen? |
-adhesion/margination/pavementing
-diapedesis
-chemotaxis
-tissue invasion |
0 |
storeysl2 Wed, 08 Feb 2012 15:03:40 GMT |
|
| What are the steps in phagocytosis? |
1. recognition and adherence to PAMPs
2. engulfment
3. phagosome formation
4. fusion with lysosomal granules to form phagolysosome
5. destruction of the target |
0 |
storeysl2 Wed, 08 Feb 2012 15:03:40 GMT |
|
| What happens when monocytes are activated into macrophages? |
-activation results in increased size, plasma membrane area, glucose metabolism, number of lysosomes, and secretory products |
0 |
storeysl2 Wed, 08 Feb 2012 15:03:40 GMT |
|
| What phagocyte is slower to arrive to the site of inflammation but lasts there longer than neutrophils? |
macrophages! |
0 |
storeysl2 Wed, 08 Feb 2012 15:03:40 GMT |
|
| What do neutrophils do? |
-ingest bacteria, dead cells, and cellular debris
-release chemokins to recruit monocytes (which turn into macrophages) |
0 |
storeysl2 Wed, 08 Feb 2012 14:59:41 GMT |
|
| What is the first phagocyte to arrive? |
neutrophil |
0 |
storeysl2 Wed, 08 Feb 2012 14:59:41 GMT |
|
| What are some examples of phagocytes? |
neutrophils, macrophages, dendritic cells |
0 |
storeysl2 Wed, 08 Feb 2012 14:59:41 GMT |
|
| Where do phagocytic cells reside? |
At points of entry such as skin and mucous membranes. |
0 |
storeysl2 Wed, 08 Feb 2012 14:59:41 GMT |
|
| process by which a cell ingests and disposes of foreign material |
phagocytosis |
0 |
storeysl2 Wed, 08 Feb 2012 14:57:43 GMT |
|
| What is the major process in innate immunity? |
phagocytosis |
0 |
storeysl2 Wed, 08 Feb 2012 14:57:43 GMT |
|
| What does interferon do? |
-protects against viral infections
-produced and released by virally infected host cells
-recruit cells that help against viral invasion |
0 |
storeysl2 Wed, 08 Feb 2012 14:57:43 GMT |
|
| What do interluekins do? |
-enhance bacteriocidal capabilities
-direct t helper cell differentiation
-stimulate proliferation
-stimulate inflammation
-suppress the immune response |
0 |
storeysl2 Wed, 08 Feb 2012 14:57:43 GMT |
|
| What are some examples of cytokines? |
-interleukins (IL)
-Interferon (IFN)
-TNF alpha
-growth factors |
0 |
storeysl2 Wed, 08 Feb 2012 14:55:20 GMT |
|
| What do cytokines do? |
-recruit
-cell proliferation and differentiation
-systemic effects
-assist in immune response, healing, phagocytosis, inflammation, defense against pathogens/cancer |
0 |
storeysl2 Wed, 08 Feb 2012 14:55:20 GMT |
|
| Low-moelcular weight, glycoproteins that are secreted by most cells |
cytokines |
0 |
storeysl2 Wed, 08 Feb 2012 14:55:20 GMT |
|
| What cytokine is important in fever? |
TNF-alpha |
0 |
storeysl2 Wed, 08 Feb 2012 14:55:20 GMT |
|
| What does the kinin system do? |
-augments inflammation
-main end point:bradykinin (vasodilation, smooth muscle permeability, pain, leukocyte chemotaxis) |
0 |
storeysl2 Wed, 08 Feb 2012 14:53:05 GMT |
|
| What does the clotting system do? |
-prevents the spread of infection and stops bleeding
-keeps microorganisms and foreign bodies at the side of greatest inflammatory cell activity
-provides a framework for repair and healing
-chemotactic for neutrophils
-enhance bradykinin (vascular permeability) |
0 |
storeysl2 Wed, 08 Feb 2012 14:53:05 GMT |
|
| What tags for destruction in the complement system? |
Pathogen Opsonized (C3b), recognized by complement receptors of phagocytes |
0 |
storeysl2 Wed, 08 Feb 2012 14:53:05 GMT |
|
| What activates mast cells in the complement system? |
Anaphylatoxin (C5a) |
0 |
storeysl2 Wed, 08 Feb 2012 14:53:05 GMT |
|
| What recruits other cells to the area in the complement system? |
Chemotaxis (C5a) |
0 |
storeysl2 Wed, 08 Feb 2012 14:50:04 GMT |
|
| What directly kills in the complement system? |
Membrane Attack Complex (MAC) created by C5b |
0 |
storeysl2 Wed, 08 Feb 2012 14:50:04 GMT |
|
| What does the complement system do? |
-directly kills
-recruits other cells to the area
-activates mast cell
-tags for destruction |
0 |
storeysl2 Wed, 08 Feb 2012 14:50:03 GMT |
|
| What's the point of inflammation? |
-prevent and limit infection and further damage
-dilute toxins
-destroy bacteria
-remove cellular debris
-control bleeding
-prevent spreading
-prepare the area of injury for healing |
0 |
storeysl2 Wed, 08 Feb 2012 14:50:03 GMT |
|
| adaptive immune response, specific, slow, memory |
third line of defense |
0 |
storeysl2 Wed, 08 Feb 2012 14:45:31 GMT |
|
| innate, inflammation, phagocytosis, nonspecific, fast, no memory |
second line of defense |
0 |
storeysl2 Wed, 08 Feb 2012 14:45:31 GMT |
|
| innate, mechanical/chemical barriers, nonspecific, constant, no memory |
first line of defense |
0 |
storeysl2 Wed, 08 Feb 2012 14:45:31 GMT |
|
| anything the body recognizes as “non-self” that induces an immune response |
antigens |
0 |
storeysl2 Wed, 08 Feb 2012 14:45:31 GMT |
|
| What are some possible short term complication associated with fractures? |
Fat embolism and compartment syndrome |
0 |
storeysl2 Tue, 07 Feb 2012 18:21:54 GMT |
|
| Major requirements to promote bone healing: |
stabilization and revascularization |
0 |
storeysl2 Tue, 07 Feb 2012 18:21:01 GMT |
|
| vertebral fractures typically associated with trauma |
burst fractures |
0 |
storeysl2 Tue, 07 Feb 2012 18:21:01 GMT |
|
| compression fractures usually associated with osteoporosis or degenerative arthritis |
vertebral fractures |
0 |
storeysl2 Tue, 07 Feb 2012 18:21:01 GMT |
|
| small crack in bone |
hairline fracture |
0 |
storeysl2 Tue, 07 Feb 2012 18:21:01 GMT |
|
| often seen in athletes who have repeated unusual or repeated stress and also heavy continuous weight on ankle or leg |
stress fracture |
0 |
storeysl2 Tue, 07 Feb 2012 18:17:54 GMT |
|
| broken bone caused by disease leading to weakness of the bone, may cause angular deformity, swelling(painless), or generalized bone pain |
pathologic fracture |
0 |
storeysl2 Tue, 07 Feb 2012 18:17:54 GMT |
|
| Break in the physical continuity of the bone, most often due to a twisting or bending of the bone or a severe fall or strike directly to the bone |
fracture |
0 |
storeysl2 Tue, 07 Feb 2012 18:17:54 GMT |
|
| Gout |
-inflammatory join disease
-bone erosions
-urate crystals in a tophus |
0 |
storeysl2 Tue, 07 Feb 2012 18:17:54 GMT |
|
| Rheumatoid Arthritis |
-pannus formation |
0 |
storeysl2 Tue, 07 Feb 2012 18:15:15 GMT |
|
| Osteoarthritis |
-eroded cartilage
-bone ends rub together |
0 |
storeysl2 Tue, 07 Feb 2012 18:15:15 GMT |
|
| Paget disease |
-related to genetic disregulation of osteocytes
-accelerated remodeling enlarges, disrupts and softens affected bones |
0 |
storeysl2 Tue, 07 Feb 2012 18:15:15 GMT |
|
| Osteomalacia/Rickets |
-result of vitamin D deficiency
-leads to bone deformities of long bones |
0 |
storeysl2 Tue, 07 Feb 2012 18:15:15 GMT |
|
| What does calcitonin-salmon do? |
-inhibits osteoclast activity
-requires sufficient oral intake of calcium and vitamin D |
0 |
storeysl2 Tue, 07 Feb 2012 18:12:48 GMT |
|
| What does parathyroid hormone do? |
-teriparatide (Forteo)
-synthetic
- increases activity of osteoblasts (bone formation) |
0 |
storeysl2 Tue, 07 Feb 2012 18:12:48 GMT |
|
| What do Selective Estrogen Receptor Modulators (SERMS) do? |
-raloxifene (Evista)
-estrogen-like effects on bone (increased bone density) and lipid decreased LDL)
-antiestrogenic in uterus and breast |
0 |
storeysl2 Tue, 07 Feb 2012 18:12:48 GMT |
|
| What do oral bisphosphonates do? |
"end in dronate"
-act to reduce bone resporption by osteoclasts
-must be accompanied by adequate intake of calcium and Vit D |
0 |
storeysl2 Tue, 07 Feb 2012 18:12:48 GMT |
|
| Steps in the bone repair process: |
1. Inflammation/hematoma formation (within hours)
2. Procallus formation (within days)
3. Callus formation (within weeks)
4. Callus replacement (up to a year or more)
5. remodeling |
0 |
storeysl2 Tue, 07 Feb 2012 18:03:05 GMT |
|
| Risk factors for fractures include: |
-adolescent age group
-spinal cord injuries
-male gender
-use of glucocorticoid medications |
0 |
storeysl2 Tue, 07 Feb 2012 18:03:05 GMT |
|
| Why is bone remodeling lengthened as you get older? |
increased osteoclast activity relative to osteoblast activity |
0 |
storeysl2 Tue, 07 Feb 2012 17:58:32 GMT |
|
| What is a key feature associated with Compartment Syndrome? |
fascia tissues do not expand |
0 |
storeysl2 Tue, 07 Feb 2012 17:58:32 GMT |
|
| Thick layers of connective tissue that contribute to the physical support and structure of the body. |
Fascia |
0 |
storeysl2 Tue, 07 Feb 2012 17:58:32 GMT |
|
| What is the largest tendon in the human body? |
Achilles tendon |
0 |
storeysl2 Tue, 07 Feb 2012 17:58:32 GMT |
|
| damage to a tendon |
strain |
0 |
storeysl2 Tue, 07 Feb 2012 17:56:17 GMT |
|
| Connect muscle to bone |
tendons |
0 |
storeysl2 Tue, 07 Feb 2012 17:56:17 GMT |
|
| What innervates the diaphragm? |
Phrenic nerve |
0 |
storeysl2 Tue, 07 Feb 2012 17:56:17 GMT |
|
| In order to live without "life support," what one skeletal muscle must function? |
Diaphragm! |
0 |
storeysl2 Tue, 07 Feb 2012 17:56:17 GMT |
|
| Why is the ACL much more likely to be torn in women than in men? |
different hip structure |
0 |
storeysl2 Tue, 07 Feb 2012 17:54:09 GMT |
|
| damage to a ligament |
sprain |
0 |
storeysl2 Tue, 07 Feb 2012 17:54:09 GMT |
|
| Control the functional movement of a joint by stretching and then returning to the usual length |
ligaments |
0 |
storeysl2 Tue, 07 Feb 2012 17:54:09 GMT |
|
| What are the components of a freely moveable joint? |
-joint capsule
-synovial membrane
-synovial fluid
-cartilage |
0 |
storeysl2 Tue, 07 Feb 2012 17:54:09 GMT |
|
| Connect bone to bone |
ligaments |
0 |
storeysl2 Tue, 07 Feb 2012 17:52:20 GMT |
|
| Decreased absorption or increased excretion of calcium means: |
bone stores of calcium will be used to maintain serum calcium levels at normal. |
0 |
storeysl2 Tue, 07 Feb 2012 17:52:20 GMT |
|
| What decreases calcium absorption in the gut? |
Ingestion of supplements >500mg of elemental calcium at one time. |
0 |
storeysl2 Tue, 07 Feb 2012 17:52:20 GMT |
|
| What drugs decrease calcium excretion in the kidneys? |
Loop diuretics (furosemide) and calcitonin |
0 |
storeysl2 Tue, 07 Feb 2012 17:52:20 GMT |
|
| How does calcium exit the body? |
via the kidneys, also fecal losses, insensible losses from breathing and sweat, manufacture of nails and hair, lactation |
0 |
storeysl2 Tue, 07 Feb 2012 17:49:34 GMT |
|
| Where is 98% of calcium stored? |
In bone tissue. |
0 |
storeysl2 Tue, 07 Feb 2012 17:49:34 GMT |
|
| Decreases serum calcium levels |
Calcitonin |
0 |
storeysl2 Tue, 07 Feb 2012 17:49:34 GMT |
|
| Increases serum calcium levels |
Parathyroid hormone |
0 |
storeysl2 Tue, 07 Feb 2012 17:49:34 GMT |
|
| What is required since bone cells are responsive to mechanical stress and micro-traumas? |
Bone remodeling |
0 |
storeysl2 Tue, 07 Feb 2012 17:47:06 GMT |
|
| Resorb bone |
Osteoclasts |
0 |
storeysl2 Tue, 07 Feb 2012 17:45:32 GMT |
|
| Terminally differentiated osteoblasts embedded in mineralized bone, they direct timing and location of remodeling, have important roles in bone stress. |
Osteocytes |
0 |
storeysl2 Tue, 07 Feb 2012 17:45:32 GMT |
|
| Derived from the hemtopoietic monocyte-macorphage lineage, possessing similar immune mechanisms |
Osteoclasts |
0 |
storeysl2 Tue, 07 Feb 2012 17:45:32 GMT |
|
| Derived from stromal cells that produce collagen, differentiate into osteocytes |
Osteoblasts |
0 |
storeysl2 Tue, 07 Feb 2012 17:45:32 GMT |
|
| Where is bone marrow found? |
Skull, pelvis, sternum, ribs. |
0 |
storeysl2 Tue, 07 Feb 2012 17:43:55 GMT |
|
| What kind of cells does bone marrow contain? |
Pluripotent (immature) stem cells |
0 |
storeysl2 Tue, 07 Feb 2012 17:43:55 GMT |
|
| If a force is applied to the cranium in older adults, where will the trauma be located? |
On the opposite side from the applied force. |
0 |
storeysl2 Tue, 07 Feb 2012 17:43:55 GMT |
|
| If a forced is applied to the cranium in a newborn, where will the trauma be located? |
Immediately below the location of the applied force. |
0 |
storeysl2 Tue, 07 Feb 2012 17:43:55 GMT |
|
| Cancelous bone that comprises 15% of the skeleton. 25% replaced annually. |
Spongy bone |
0 |
storeysl2 Tue, 07 Feb 2012 17:41:16 GMT |
|
| Cortical bone that comprises 85% of the skeleton. 3% replaced annually. |
Compact bone |
0 |
storeysl2 Tue, 07 Feb 2012 17:41:16 GMT |
|
| What covers the bones? |
Periosteum |
0 |
storeysl2 Tue, 07 Feb 2012 17:41:16 GMT |
|
| Bones function to: |
-Serve as storage site for minerals
-Serve as a site for formation of blood cells
-Provide protection of organs |
0 |
storeysl2 Tue, 07 Feb 2012 17:41:16 GMT |
|
