Cell Death MCQs

Necrosis is characterized by changes in the cytoplasm and nuclei of the injured cells. Necrotic cells show increased eosinophilia(i.e., they are stained red by the dye eosin), attributable partly to increased binding of eosin to denatured cytoplasmic proteins and partly to loss of basophilic ribonucleic acid(RNA) in the cytoplasm(basophilia stems from binding of the blue dye hematoxylin). Compared with viable cells, the cell may have a glassy, homogeneous appearance, mostly because of the loss of lighter staining glycogen particles. Myelin figures are more prominent in necrotic cells than in cells with reversible injury. When enzymes have digested cytoplasmic organelles, the cytoplasm becomes vacuolated and appears "moth-eaten." Reference: Robbins and Cotran Pathologic Basis of Diseases, 10 th ed Pg:35

Anti-apoptotic. BCL2, BCL-XL, and MCL1 are the principal members of this group; they possess four BH domains (called BH1-4). These proteins reside in the outer mitochondrial membrane as well as in the cytosol and ER membranes. Regulated apoptosis initiators or sensors. Members of this group, including BAD, BIM, BID, Puma, and Noxa, contain only one BH domain, the third of the four BH domains, and hence are sometimes called BH3-only proteins. The activity of BH3-only proteins is modulated by sensors of cellular stress and damage; when upregulated and activated, they can initiate apoptosis. Reference: Robbins& Cotran Pathologic Basis of Diseases 10 th edition, Chapter - 2 pg 44

In most tissues, the main histologic finding associated with infarcts is ischemic coagulative necrosis. Coagulative necrosis is a type of cell death that occurs when blood flow to cells stops or slows (ischemia). It can occur anywhere in the body except the brain. Many conditions can cause ischemia, including atherosclerosis. Treatment and prognosis depend on the extent of the damage to the cells and tissues. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:115

At autopsy, postmortem clots can sometimes be mistaken for venous thrombi. However, the former are gelatinous and because of red cell settling they have a dark red dependent portion and a yellow "chicken fat" upper portion; they also are usually not attached to the underlying vessel wall. By contrast, red thrombi typically are firm, focally attached to vessel walls, and they contain gray strands of deposited fibrin. Reference: Robbins and Cotran Pathologic Basis of Diseases, 10ᵗʰ ed Pg:110

Communicating junctions (Gap junctions) mediate the passage of chemical or electrical signals from one cell to another. Consists of pores called connexions and formed by hexamers of transmembrane proteins called connexins. Reference: Robbins 9th/pg 11

Intermediate filaments are 10-nm diameter fibrils which provide tensile strength to a cell. Cadherins are cell-cell desmosomal junctions that are formed by homotypic association of transmembrane glycoproteins. Reference: Robbins 9th/pg 21-24

In heterozygotes approximately 40% of Hb is HbS and the remainder is HbA, which interacts only weakly with deoxygenated HbS. Because HbA greatly retards HbS polymerization, the red cells of HbS heterozygotes have little tendency to sickle in vivo. Such persons are said to have sickle cell trait. On electrophoresis, 2 bands are produced. In homozygous state, most of all hemoglobins are HbS. So, single band is produced. Reference: Robbins, 10 th edition, page number - 445

PAN is characterized by segmental transmural necrotizing inflammationQ frequently accompanied by fibrinoid necrosis.Q OPTION B, C, D are granulomotous vasculitis. Reference : Robbins 9th/pg 509; 8th/pg 511