An aids patient complains o headaches and disorietation. A clinical diagnosis of Toxoplasma encephalitis is made and toxoplasma cysts are observed in a brian section. Which of the following antibody results would be most likely in this patient?
A.)igM nonreactive,igG nonreactive
B.)igM nonreactive,igG(low titer)
c.)igM reactive (low titer),igG reactive (high titer)
D.)igM reactive (high titer),igG reactive (high titer)
E.)igM reactive (high titer),igG nonreactive
An aids patient complains o headaches and disorietation. A clinical diagnosis of Toxoplasma encephalitis is made and toxoplasma cysts are observed in a brian section. Which of the following antibody results would be most likely in this patient?
A.)igM nonreactive,igG nonreactive
B.)igM nonreactive,igG(low titer)
c.)igM reactive (low titer),igG reactive (high titer)
D.)igM reactive (high titer),igG reactive (high titer)
E.)igM reactive (high titer),igG nonreactive
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A 26-year-old woman presented with painful, stiff knees of 4 weeks duration. She had a 6-year history of Raynaud's phenomenon. On examination, she had bilateral effusions in both knee joints, but all other joints were normal. She had no skin lesions, muscle tenderness, proteinuria or fever. The results of relevant investigations are shown in Table C10.1. On the basis of these, a diagnosis of Systemic Lupus Erythematosus (SLE) was made and the patient treated with aspirin for her painful knees. She improved over 4 weeks and then remained symptom-free for 5 years. During this time, her antinuclear antibody remained positive at 1/80, her DNA-binding activity varied from 40 to 80%, and her C3 and C4 levels were occasionally low. Later, she developed a bilateral, butterfly rash across her cheeks, blotchy rash on her hands and thighs, consistent with active vasculitis and also presented with proteinuria, hematuria and glomerular nephritis. Her Raynaud's phenomenon concurrently became much worse. Following treatment with prednisolone, the skin manifestations gradually disappeared and the steroids were tailed off.
This patient presented with arthritis and Raynaud's phenomenon. She is unusual in that the arthritis of SLE usually involves small joints, but it is important to note that she remained perfectly well without treatment for 5 years, despite persistently abnormal serology.
Table C10.1 Investigations in Case 10.8.
C-reactive protein | 8mg/l (normal) |
Rheumatoid factor | Negative |
Antinuclear antibody | Positive (titer 1/80; IgG class) |
dsDNA-binding activity | 80% (NR 0-30% binding) |
Antibodies to extractable nuclear antigens | Negative |
Serum complement levels | |
C3 | 0.35g/l (NR 0.65-1.30) |
C4 | 0.05g/l (NR 0.20-0.50) |
Serum immunoglobulins | |
IgG | 22.0g/l (NR 7.2-19.0) |
IgA | 3.8g/l (NR 2.0-5.0) |
IgM | 1.2g/l (NR 0.5-2.0) |
Biopsy of normal, sun-exposed skin (lupus band test) | Granular deposits of IgG and complement at dermo-epidermal junction |
1) Explain the immunological basis of her disease condition and the significance of her elevated levels of antinuclear antibodies (ANA).
2) Explain as to what caused her glomerular nephritis, vasculitis and bilateral skin rash.
3) How would you categorize the type of hypersensitivity reactions causing the above disease?
4) Explain how prednisolone helped to treat the symptoms.
5) Explain the biochemical mechanism of action of aspirin in its interaction with cyclooxygenase. Which class of macromolecules are affected by this interaction (inhibition) and state briefly a major side effect that may develop as a result of extensive aspirin therapy.
Patient
32 year-old female with a history of poly-substance abuse, including IV drug use, who presented at the ER with fever, abdominal pain, nausea, vomiting, headaches and myalgia (muscle pain). She also had toothache for which she had taken approximately 50 acetaminophen tablets over a 24 hour period. She was transferred to a medical center ER for the acetaminophen overdose.
Physical exam showed patient alert and oriented with normal vital signs. Right upper quadrant pain was noted, as well as mild jaundice.
Diagnostic
Laboratory testing indicated the following liver function tests and other tests:
AST | ALT | GGT | LDH | BUN | Creatinine | Acetaminophen |
791 U/liter | 1,398 U/liter | 166 U/liter | 826 U/liter | 83 mg/dl | 10.1 mg/dl | 15µg/ml |
Hepatitis A IgM | Hepatitis A IgG | Hepatitis B Surface Antigen | Hepatitis B Surface Antibody | Hepatitis B Core IgM | Hepatitis C Total (IgM/IgG) |
Negative | Negative | Negative | Negative | Negative | Positive |
Her hospital course was significant for acute renal and liver failure, with improvement after dialysis was performed.
Based on the patientâs history, presenting symptoms and LFT results, which of the following viruses would be most likely to be the problem?
BK virus
JC virus
Hepatitis B or C
CMV
After reviewing the serologic test results, which organism is the causative virus?
Hepatitis B
Hepatitis C
Hepatitis A
Hepatitis D
What are the modes of transmission for this virus? Which was most likely in this case?
Based on how she was infected, would she be at risk for any other viral infections? Which ones?
Why would it be important to determine the genotype of the virus with which she is infected?
If she had received a vaccination for the virus, would this infection have been prevented? Why or why not?
please i need an answer for all of these questions. this is due 10/19.