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Concept of Infection and Psychiatric Disorders - Essay Example

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The paper "Concept of Infection and Psychiatric Disorders" tells that since IgA deficiency is a pathologic condition, it is important to be certain in the diagnosis of the condition. It is suggested to obtain another sample, and measure the immunoglobulins again to verify the initial findings…
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Concept of Infection and Psychiatric Disorders
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CASE Question Yes, because six calibration solutions were used to make the calibration curve, which is the recommended number for calibrating nephelometers (Blirup-Jensen, 2001). Question 2: IgG concentration is 15.2 g/L, IgA concentration is 0.0 g/L, and IgM concentration is 0.70 g/L. Question 3: Since IgA deficiency is a pathologic condition, it is important to be certain in the diagnosis of the condition. It is suggested to obtain another sample, and measure the immunoglobulins again to verify the initial findings. If the same results will be obtained again, then the diagnosis is established. Question 4: The patient is a 50 year old male, with a chief complaint of recurrent respiratory infection since he was a teenager, resulting to annual antibiotics use. No family history of respiratory illness, and no personal history of smoking. Final diagnosis is primary immunoglobulin A deficiency (IgAD). Question 5: A wide array of diseases, such as infection and psychiatric disorders, can be mistakenly associated with IgAD, because certain medications for these conditions cause transient IgA depletion. Drugs, such as D-penicillamine, Sulfasalazine, Aurothioglucose, Fenclofenac, Gold, Captopril, Zonisamide, Phenytoin, Valproic Acid, Thyroxine, Chloroquine, Carbamazepine, Hydantoin, Levamisole, Ibuprofen, Salicylic acid, and Cyclosporin A can cause transient IgAD. Thus, history of medications is an important part of initial assessment among patients presenting with IgAD. Drug-induced IgAD can be verified by the return of IgA to normal levels once intake of the culprit drug is stopped (Dolina, 2011). In addition, infections like Rubella, Cytomegaloviruses, Toxoplasma gondii, and Epstein-Barr virus may also cause transient IgAD. The most effective management of IgAD in this case will be the resolution of the infection (Dolina, 2011). Finally, bone marrow transplantation from an IgA-deficient donor may also cause IgAD to the recipient. History of bone marrow transplantation and IgAD in the donor after the said surgical procedure point to acquired IgAD. It is thus important to thoroughly screen the donors before proceeding with the transplant (Dolina, 2011). Question 6: Recurrent ear infections such as otitis media, sinopulmonary infections such as pneumonia and tonsillitis, GI tract infections, severe allergic reaction following blood products transfusions, or, in children, failure to thrive are all possible complications of IgAD (Dolina, 2011). CASE 2 Question 8: IgG concentration is 2.7 g/L, IgA concentration is 1.8 g/L, and IgM concentration is 0.70 g/L. Question 9: It can be seen that alpha 1 (α1) and 2 (α2) globulins are elevated, and the albumin percent and levels decreased. On the other hand, levels of beta (β) and gamma (γ) globulins are within normal values. Question 10: Presence of albumin, as well as α1-, α2-, β-, and γ -globulins was detected in immunofixation. The single band of γ-globulin is a sign of its monoclonality, in contrast to others which are polyclonal. This is an abnormal finding. In addition, positive staining with anti-µ and anti-λ antibodies denotes that the single band is a µ-λ monoclonal immunoglobulin. Question 11: The concentration of monoclonal γ-globulin is 9.3 g/L. Question 12: The presence of back pain, anemia and monoclonal immunoglobulin points to multiple myeloma (MM). Other differential diagnoses are primary amyloidosis, malignant lymphoma, monoclonal gammopathies of undetermined significance (MGUS), Waldenstrom hypergammaglobulinemia (Seiter, 2012), post-transplant monoclonal gammopathies, hepatitis C or HIV infection, systemic lupus erythematous (SLE), rheumatoid arthritis, psoriatic arthritis, Sjogren’s syndrome, and Schnitzler’s syndrome (Anon., 2011). Question 13: Bone marrow aspiration and biopsy is suggested to verify or to rule out malignancy. Histologic analysis can also help differentiate MM with Waldenstrom hypergammaglobulinemia, which presents with lymphoplasmacytic infiltration of bone marrow instead of plasma cell infiltration seen among MM patients (Seiter, 2012). The extent of hematologic abnormalities can be determined by complete blood count and peripheral blood smear, which can verify anemia, and identify presence of Rouleau bodies, thrombocytopenia, leukopenia, pancytopenia, abnormal coagulation, or elevated erythrocyte sedimentation rate (Seiter, 2012). To check for degree of renal impairment, metabolic assessment of blood urea nitrogen (BUN), creatinine and uric acid levels should also be done. 24-hour urine collection to determine creatinine clearance and urine protein levels can also establish diagnosis, as > 1 g urine protein in 24 hours is a major criterion for MM diagnosis. It may also show low reticulocyte count. Aside from renal function tests and globulin measurements, measurement of β-2 microglobulin can also help determine whether the case is a primary renal insufficiency (increased β-2 microglobulin) or MM (Seiter, 2012). Skeletal survey, Positron Emission Tomography (PET) scan and Magnetic Resonance Imaging (MRI) should also be done to determine the extent of bone pathology caused by the disease. To prognosticate MM, renal function, C-reactive protein levels and cytogenetics should be analyzed (Seiter, 2012). Question 14: MGUS is the most common monoclonal gammopathy, found in about 1% to 2% of adults (Anon., 2011). CASE 3 Question 15: This is a reasonable request, because CD4 level is an important factor in predicting the effectiveness of highly active antiretroviral therapy (HAART). As reported by Levin (2006), several studies have found that HAART is more effective when initiated at higher CD4 levels. In particular, CD4 levels of greater than 350 cells returned to near normal CD4 levels after therapy. As well, measurement of CD4 level is an important measure of the effect of HAART. Question 16: a) Since the tube 1 cells in region A of CD45 vs. SSC dot plot are CD45-positive, then they are leukocytes (Becton-Dickinson, n. d.). b) The intense signaling of tube 1 cells in quadrant 2 of CD3 vs. CD4 dot plot signifies that those cells are both CD3- and CD4-positive, which means that they are helper T lymphocytes (Becton-Dickinson, n. d.). c) On the other hand, detection of tube 1 cells in quadrant 2 of CD3 vs. CD8 dot plot indicates that those cells are both CD3- and CD8-positive, suggesting that they are cytotoxic T lymphocytes (Becton-Dickinson, n. d.). d) Analyzing cells in tube 2, those found in quadrant 1 of CD56 vs. CD3 dot plot are both CD56-positive and CD3-negative, and such cells are natural killer cells (Cytognos SL, 2010). e) In contrast, the cells in quadrant 2 of the same dot plot as that in (d) are both CD3- and CD56-positive. This means these cells are Natural Killer T cells (Koreck et al., 2002) f) Meanwhile, the cells in quadrant 3 of the same dot plot used in (d) and (e) are both CD3- and CD56 negative. This means that they can either be CD45-positive leukocytes (Becton-Dickinson, n. d.), or CD19-positive B lymphocytes (Cytognos SL, 2010). g) Conversely, cells in quadrant 4 of CD56 vs. CD3 dot plot of are both CD3-positive and CD56-negative, which is characteristic of mature human T lymphocytes (Becton-Dickinson, n. d.). h) The tube 2 cells in quadrant 1 of CD3 vs. CD19 dot plot are both CD19-positive and CD3-negative. Such combination of clonal differentiating proteins is found among B lymphocytes (Cytognos SL, 2010). i) On the other hand, the tube 2 cells in quadrant 4 of the same dot plot as that in (h) are both CD3-positive and CD19-negative, which means that they are mature human T lymphocytes (Becton-Dickinson, n. d.). j) Finally, the intensely signaling elements in region I of plot 7cytogram of tube 2 are absolute count beads (Becton-Dickinson, n. d.). Question 17: Knowing about the amount of beads that have been added to the tubes is necessary to accurately calculate the number of cells measured through flow cytometry. As well, clear and sterile reagent and sample solutions should be used to increase quality of flow cytometry, as precipitation, discoloration and contamination compromise the process. Because of this, fresh preparation of anti-coagulated blood should be stained within 48 hours of draw, and analyzed within 24 hours after staining (Becton-Dickinson, n. d.). Question 18: The patient on HAART is found to still have depleted number of Helper T cells. Helper T cell absolute and relative count is 190 cells/µl and 19%, respectively. Based on reference ranges established by three clinical investigation centers in United States that measured the absolute and relative lymphocyte count among hematologically normal adults between ages 18 and 65 years, these are low, since the determined normal range of absolute and relative values are 404-1612 cells/µl and 33-58%, respectively (Becton-Dickinson, n. d.). Question 19: The immunofluorescence image shows presence of anti-neutrophil cytoplasmic antibodies (C-ANCA) in the neutrophil, seen among patients with Wegener Granulomatosis, which also manifests with episodes of epistaxis, as well as respiratory and renal failure (Papadoupoulos, 2011). Question 20: Lethargy, fatigue, generalized pruritus, and abnormal liver function tests are signs of autoimmune hepatitis (AIH). The type of autoantibodies present depends on the type of AIH. Anti-smooth muscle (ASMA) and antinuclear (ANA) antibodies are found in AIH-1, anti-liver-kidney microsomal type 1 (anti-LKM-1) antibody in AIH-2, and anti-soluble liver antigen antibody (anti-SLA) in AIH-3 (Wolf, 2011). Question 21: Fatigue, arthralgias, renal impairment, and malar rash in a young female are the classical clinical presentation of systemic lupus erythematosus. The autoantibodies present in this condition are ANA, which is used as a highly-sensitive screening test among suspected patients, anti-dsDNA, which is a specific screening tool, anti-SM, anti-SSA or anti-SSB, anti-ribosomal P, anticardiolipin, and anti-histome antibodies (Bartels, 2011). Question 22: Comparison of direct and indirect immunofluorescence (Anon., n.d.) Direct immunofluorescence Indirect immunofluorescence What is its objective? Identify the infecting organism Identify unknown serum species-specific antibody What is added to sera? Known mixture of fluorescently-labeled antibodies against family- and species-specific antigens. Organism of known species Are there additional reagents? None A fluorescently-tagged anti-human antibody When is it used? Performed when multiple species of bacteria infect a host when low number of infecting bacteria are suspected What is the clinical presentation of the patients undergoing this test? Symptomatic patients asymptomatic patients What is the clinical presentation of the patients undergoing this test? Increased antibody concentration in serum Low levels of serum antibodies What is an example of clinical conditions where this is applicable? Differentiating Neisseria gonnorhoeae and Treponema pallidum infections which have similar clinical presentations. At the infection stage of N. gonnorrhoeae infection. REFERENCES Bartels, C. M., 2011. Systemic Lupus Erythematosus (SLE). [online] Available at: [Accessed 28 April 2012] Becton-Dickinson, n. d. MultiTEST CD3 FITC/CD8 PE/CD45 PerCP/CD4 APC Reagent. U. S. Pat. 4, 520, 110. Cytognos SL, 2010. CD56-FITC / CD19-PE / CD3-PECy5. Spain: Cytognos SL. Dolina, M. Y., 2011. Immunoglobulin A Deficiency. [online] Available at: [Accessed 28 April 2012] Koreck, A. et al., 2002. CD3+CD56+ NK T cells are significantly decreased in the peripheral blood of patients with psoriasis. Clin Exp Immunol, 127(1), pp. 176-182. Levin, J., 2006. Starting HAART Earlier Results in Highest CD4 Count. [online] Available at: [Accessed 28 April 2012] Papadoupoulos, P. J., 2011. Wegener Granulomatosis. [online] Available at: [Accessed 28 April 2012] Seiter, K., 2012. Multiple Myeloma. [online] Available at: [Accessed 28 April 2012] Wolf, D. C., 2011. Autoimmune Hepatitis. [online] Available at: [Accessed 28 April 2012] 2011. Assessment of Monoclonal Gammopathies. [online] Available at: [Accessed 28 April 2012] Immunofluorescence Tutorial. [online] Available at: [Accessed 28 April 2012] Read More
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