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CongratulatoryHeisenberg

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Kirkuk University - Faculty of Pharmacy

Dr.mohanad muhsin

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cell injury pathology cell biology medical science

Summary

This document discusses cell injury and degeneration, covering different types of cell injury and their causes, along with different types of cell adaptations like hypertrophy, hyperplasia, atrophy, and metaplasia, and types of necrosis. It's targeted at third-year pharmacy students, possibly part of a lecture or learning material.

Full Transcript

Cell injury and degenerations Kirkuk university-faculty of pharmacy Pathophysiology-practical 3rd stage By dr.mohanad muhsin Cell injury: results when cells are stressed so severally that no logger able to adapt or when cells are exposed to inheriting damaged agent or suffering from int...

Cell injury and degenerations Kirkuk university-faculty of pharmacy Pathophysiology-practical 3rd stage By dr.mohanad muhsin Cell injury: results when cells are stressed so severally that no logger able to adapt or when cells are exposed to inheriting damaged agent or suffering from intrinsic abnormality. *Result of cell injury: non lethal injurious agents Reversible cell injury (degeneration) Metabolic and morphological change in a tissue lethal injurious agents Irreversible cell injury (cell death) -Necrosis :un programmed death of group of cells within a living body. -Programmed cell death(apoptosis) necrosis of single cell in a living tissue. *Causes of cell injury -hypoxia (reduced oxygen) & ischemia (insufficient blood flow ). -chemical agent -physical agent -infectious agent -nutritional disturbances -immunological reaction -Hypertrophy : is an increase in the size of the cells resulting in increase in size of organ. -Hyperplasia: is an increase in the number of the cells resulting increase in size of the organ. -Atrophy :it is a decrease in the size of the cells resulting in decrease in size of the organ (shrinkage of tissue or organ ). -Metaplasia: transformation of one differentiated cell type to another differentiated cell type (replacement in the type of cells ). Cardiac hypertrophy, gross The number of myocardial fibers does not increase , but their size can increase in response to an increased workload, leading o marked thickening of the LV. Increased pressure load cause of left ventricular hypertrophy. Testis, atrophy, gross On the left is a normal testis, and the testis on the right has undergone atrophy. May occur with various conditios,including chronic alcoholism, atherosclerosis , Chemotherapy or radiation. Normal prostate & Prostatic hyperplasia, gross This 5-cm diameter prostate is enlarged and nodular as a result of prostatic Hyperplasia. This is a process that occurs gradually over many years, typically After age 50 y. An enlarged prostate can obstruct urinary outflow from the bladder and lead to an obstructive uropathy. Barret esophagus, gross & microscopic Chronic GERD( gastro esophaygeal Reflux Disease) lead to metaplasia of the normal esophageal squamous mucosa into gastric-type columnar mucosa. Necrosis :death of group of cells with a living body. Types of necrosis * cogulative * liquefaction * caseous * fat * fibrinoid Coagulative necrosis Most common type, mostly from sudden cessation of blood flow(ischemia). The organs commonly affected are the heart, kidney and spleen This axial section reveals a large MI involving the anterior Lt ventricular wall and Interventricular septum in distribution of the left anterior descending coronary artery Yellowish area of necrosis with the hyperemic border Note the wedge shape of this acute infract, with the pale zone of coagulative Necrosis result from loss of blood supply with resultant tissue ischemia that Progresses to infraction. Caseous necrosis It is type od necrosis seen in the tuberculous infections , it combines features of Both coagulative and liquefactive necrosis, term “caseous ” cheese-like. Tuberculosis lung Large nodules may have central caseous necrosis that includes elements of liquefactive and coagulative necrosis. Liquefaction necrosis : It is a type of necrosis which result in transformation of The tissue into liquid viscous material due ischemic injury and bacterial infection. In this coronal section , a subacute infract of the frontal lobe shows liquefactive Necrosis with beginning formation of cystic space are resolution occurs 10 days to 2 weeks after the initial ischemic event. Microscopic picture, liquefactive necrosis of brain On the right are many macrophages( ) that are present in this subacute infract to phagocytize lipid debris from the ongoing liquefactive necrosis. Focal ischemic infraction (stroke) can result from either arterial thrombosis or embolism.

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