Showing posts with label PATHOLOGY. Show all posts
Showing posts with label PATHOLOGY. Show all posts

Sunday, 15 February 2015

HIGH YIELD POINT FOR PATHOLOGY 2015

HIGH YIELD POINT FOR PATHOLOGY  2015

http://www.doctorsquiz.com important topics for DNB-CET, AIPGMEE, FMGE, DNB-PDCET, UPSC-CMS online medical examination .



1. Fastest growing tumor – Burkitt’s

2. PE’s are found in half of all autopsies

3. Courvoisier’s Law: tumors that obstruct the common bile duct cause enlarged gallbladders, but obstructing

gallstones do not (too much scarring), so if you can palpate the gallbladder you’e probably looking at cancer.

4. Only DNA virus to replicate in cytoplasm: Pox

5. Only RNA virus to replicate in nucleus: Influenza

6. Bacillus anthracis has the only protein capsule

7. Bordetella pertussis (Whooping Cough) elicits lymphocytosis rather than granulocytosis

8. Bronchioalveolar carcinomas grow without destroying the normal architecture of the lung

9. Cryptococcus neoformans often lacks a capsule and, when stained with GMS, looks just like Pneumycistis

carinii, except that Cryptococcus lacks the prominent nucleoli.

10. Weil Felix reaction: (+)R. rickettssi & (+)Proteus vulgaris & P. mirabilis

11. Treponema pallidum (Syphilis) tests: 1)VDRL 2)FTA-Abs: most widely used 3)TPI (immobilization test – most expensive but the Gold Standard)

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Wednesday, 4 February 2015

HIGH YIELD POINT FOR PATHOLOGY 2015



HIGH YIELD POINT FOR PATHOLOGY 2015


http://www.doctorsquiz.com important topics for DNB-CET, AIPGMEE, FMGE, DNB-PDCET, UPSC-CMS online medical examination .
.    

Human leukocyte antigens and different classes:


The human leukocyte antigen system (HLA) is the name of the major histocompatibility complex


(MHC) in humans. It is located on chromosome 6. Two different classes.


HLA class 1 [MHC-1]: HLA-A, HLA-B, HLA-C


HLA class 2 [MHC-2]: HLA-DP, HLA-DQ, HLA-DR


Location of MHC-1 & MHC-2 antigens:


MHC-1: All nucleated cells & platelets (NO MHC on RBC)


MHC-2: Antigen Presenting cells (Dendritic cells, langerhans cells, activated macrophage, B-cells, activated T-cells & activated endothelial cells)


Important-


MHC-1 is necessary for antigen recognition by CD8+ T-cells


MHC-2 is necessary for antigen recognition by CD4+ T-cells
Difference:


MHC-1: React with ENDOGENOUSLY produce peptides by virus, intracellular bacteria, intracellular parasites and tumor cells


MHC-2: React with EXOGENOUSLY PROCESSED antigens


Handling of organisms:


MHC-1: It works with intracellular organisms so after reacting with endogenously processed antigen, β2


microglobulin transports MHC class-1 molecules to the cell surface where it can be recognized by CD 8


T-cells and organisms are then killed by CD8 T-cells


MHC-2: It works with Extracellular organisms so once organisms engulfed, MHC class-2 molecule fuse with vacuole containing exogenously processed antigen, invariant chain is released and MHC-2-peptide complex is then transported to the cell surface where it can be recognized by CD 4 T-cells. Invariant chain prevents interaction b/w endogenously produced peptide and MHC-2 molecules intracellularly


How does ADCC [Antibody Dependent Cellular Cytotoxicity] and NK cells mediated cytotoxicity differed?


ADCC: IgG + NK cells → use CD 16 molecule (Fc receptor) to identify target cells.


NK cells mediated cytotoxicity: use CD 56 (No antibody involve Ex.- lysis of infected RBC)


Complement system:



Classical Pathway:
activated by antigen-Ab reaction (IgG & IgM, IgM most efficient) [start point C1] [C1 - C4 - C2 - C3] [C4bC2a is C3-convertase] [C4bC2aC3b (C5-convertase) splits C5 into C5a & C5b which then form C5b,6,7,8,9]


Alternative Pathway: C3 hydrolyze spontaneously in our body into C3a & C3b. If there is a pathogenic membrane surface nearby, C3b binds to it. If not, both C3a & C3b rejoin. Upon binding with a cellular membrane, C3b is bound by factor B to form C3bB. This complex in presence of factor D will be cleaved into Ba and Bb. Bb will remain covalently bonded to C3b to form C3bBb which is the alternative pathway C3-convertase.