Sandbox:Akshun

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Passage 1

Coagulation necrosis is characterized by hypereosinophilia, nuclear pyknosis followed by karyorrhexis and karyolysis (total loss of nuclei and loss of cytoplasmic cross-striations). It is generally first visible in the period from 4-12 hours following infarction. Necrotic myocytes may retain their striations for a long time. Neutrophilic infiltration (acute inflammation), edema and hemorrhage are also first visible at 4-12 hours, but generally closer to 12 hours. The interstitium at the margin of the infarcted area, is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose or eat the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous or collagenous scar (which are typical steps in wound healing). The interstitial space or the space between cells outside of blood vessels may be infiltrated with red blood cells. Infiltration by macrophages, lymphocytes, eosinophils, fibroblasts and capillaries begins around the periphery at 3-10 days. Contraction band necrosis is characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes and is usually seen at the edge of an infarct or with reperfusion, for example with Thrombolytic therapy.

Passage 2

Acute Bronchitis may be caused by either Viral bacterial or environmental factor. Influenza virus is the most common overall cause, other causes of acute bronchitis are mostly viruses including;

• Respiratory syncytial virus (RSV)
• Coronavirus
• Enterovirus