The most avidly complement fixing antibody is:

a. IgA
b. IgG
c. IgM
d. IgE

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Classical complement pathway activation is denoted by:

a. C2, C4 and C3 decreased.
b. C2 and C4 normal, C3 decreased.
c. C3 normal and C2, C4 decreased.
d. C2, C4, C3 all elevated.

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All of the following are part of innate immunity except:

a. Complement.
b. NK cells.
c. Macrophages.
d. T cells

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Prozone phenomenon is due to:

a. Antigen excess.
b. Antibody excess.
c. False +ve reaction.
d. False -ve reaction.

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What enhances multiplication of T cells in culture?

a. Phytohemagglutinin.
b. Chemotactic factor.
c. Leukotrienes.
d. Prostaglandins.

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All of the following are glycoproteins except:

a. Blood antigen.
b. Albumin.
c. Immunoglobulin.
d. hCG.

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All of the following are involved in antigen antibody reaction except:

a. Van der Waals forces.
b. Electrostatic bond.
c. Hydrogen bond.
d. Covalent bond.

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Interleukin 1 produces:

a. T-lymphocyte activation.
b. Delayed wound healing.
c.. Increased pain perception.
d. Decreased PMN release from marrow.

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The serum concentration of which of the following IgG subclasses is maximum?

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a. IgG1
b. IgG2
c. IgG3
d. IgG4

All of the following are found in Primary Sjogren syndrome except:

a. Lymphoma.
b. Connective Tissue disorder.
c. Xerostomia.
d. Xeropthalmia.

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Sicca syndrome is associated with all except:

a. Midline granuloma.
b. Chronic active hepatitis.
c. Rheumatoid arthritis.
d. Scleroderma.


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Indications for steroids in SLE are all except:

a. Myocarditis.
b. Endocarditis.
c. Thrombocytopenia.
d. Neuropsychiatric symptoms.


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In which of the following arthritis, erosions are not seen:

a. Rheumatoid Arthritis.
b. Psoriasis.
c. SLE.
d. Gout.



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Autoimmune destruction of platelets is seen in:

a. SLE.
b. Rheumatoid Arthritis.
c. Reiter disease.
d. Polyarteritis nodosa.



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Antibody found in myositis is

1. Anti Jo1
2. Anti scl 70
3. Anti Sm
4. Anti Ku
   
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Malakoplakia - Wikipedia, the free encyclopedia

Malakoplakia -

Malakoplakia is a rare inflammatory condition which makes its presence known as a papule, plaque or ulceration that usually affects the genitourinary tract. However, it may also be associated with other bodily organs. It was initially described in the early 1900s as soft yellowish plaques found on the mucosa of the urinary bladder. Microscopically it is characterized by the presence of foamy histiocytes with basophilicinclusions called Michaelis-Gutmann bodies.

It usually involves gram negative bacteria.

Malakoplakia is thought to result from the insufficient killing of bacteria by macrophages. Therefore, the partially digested bacteria accumulate in macrophages and leads to a deposition of iron and calcium. The impairment of bactericidal activity manifests itself as the formation of an ulcer, plaque or papule.

Malakoplakia is associated with patients with a history of immunosuppression due tolymphoma, diabetes mellitus, renal transplantation, or because of long-term therapy with systemic corticosteroids.

Today, antibiotics are used for treatment of malakoplakia.