pathology · 19 May 2021 0

Morphologic differences between Aspergillus and mucor.

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Renal pathology quiz for NEET-SS/ DM- Oncopathology/ DM Histopathology, Fellowships, FRCPath- Histopathology and AP/CP boards

Renal pathology quiz

by pathologymcqs 12 Jun 2021

Robbins pathologic basis of disease 10th edition has a handful of changes and updates when compared to it's predecessor. Here is a brief note on the chapterwise updates which are high yield for entrance exams. **ROBBINS 10TH EDITION CHAPTERWISE UPDATES** **CHAPTER 1- CELL** * ***Satellite DNA****- A major component of centromeres is so-called satellite DNA, consisting of large arrays—up to megabases in length—of repeating sequences (from 5 bp up to 5 kb). Although classically associated with spindle apparatus attachment, satellite DNA is also important in maintaining the dense, tightly packed organization of heterochromatin. * * ***Gene Editing and CRISPR- ****An exciting new development that allows high-fidelity genome editing may usher in the next era of the molecular revolution. This advance comes from a wholly unexpected source: the discovery of clustered regularly interspaced short palindromic repeats (CRISPRs) and CRISPR-associated genes (Cas), such as the Cas9 nuclease.* **CHAPTER 2- ADAPTATIONS AND INJURY** * ***Ferroptosis- ****Only discovered in 2012, ferroptosis is a distinct form of cell death that is triggered when excessive intracellular levels of iron or reactive oxygen species overwhelm the glutathione-dependent antioxidant defenses. * **CHAPTER 3-INFLAMMATION AND REPAIR** * ***Neutrophil extracellular traps (NETs)- ****NETs were mentioned in the previous edition it is further elaborated in the latest edition. Neutrophil extracellular traps (NETs) are extracellular fibrillar networks that concentrate antimicrobial substances at sites of infection and trap microbes, helping to prevent their spread.* **CHAPTER 6- IMMUNITY** * ***Rejection of tissue transplants:*** *Elaborated compared to the previous edition*. **CHAPTER 7- NEOPLASIA** * ***A few newly added proto-oncogenes: *** 1. FMS-like tyrosine kinase 3 (FLT3) Point mutation or small duplications in Leukemia. 2. GTP-binding (G) proteins- GNAQ Point mutation in Uveal melanoma. 3. GTP-binding (G) proteins- GNAS Point mutation in Pituitary adenoma. * ***A few newly added tumor suppessor genes:*** 1. SDHB, SDHD (Succinate dehydrogenase complex subunits B and D TCA cycle, oxidative phosphorylation) seen in Familial paraganglioma, familial pheochromocytoma. * ***Elaboration of oncogenic activities of E6 an E7 proteins of human papilloma virus (HPV)*** 1. In the older edition it was mentioned that the E6 protein of HPV inactivates p53. In the 10th edition it is mentioned that in addition to inactivation of p53, E6 protein also increases telomerase expression (TERT). **CHAPTER 8- INFECTIOUS DISEASES** * *Updates on the SARSCoV2 virus*

Robbins pathologic basis of disease 10th edition updates

by pathologymcqs 11 Jun 2021

The two most common forms of human DNA variation in the human genome 1. Single nucleotide polymorphisms (SNPs) and 2. Copy number variations (CNVs). Let’s looks at a few differences between the two human DNA variations. Very important topic for examinations. Single nucleotide polymorphisms (SNVs) SNPs are variants at single nucleotide positions and are almost always biallelic. Roughly 1% of SNPs occur in coding regions. SNPs may be useful markers if they happen to be coinherited with a disease-associated polymorphism. In other words, the SNP and the causative genetic factor are in linkage disequilibrium. Copy number variations CNVs can be biallelic and simply duplicated or,deleted in some individuals. Approximately 50% of CNVs involve coding sequences. CNVs are responsible for 5 million and 24 million base pairs of sequence difference between any two individuals.

Differences between the types of human DNA variations

by pathologymcqs 11 Jun 2021

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