Anatomy and phys lecture 12
Anatomy and phys lecture 12 PHCL2600
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This 6 page Class Notes was uploaded by Legacy Tanner on Tuesday October 6, 2015. The Class Notes belongs to PHCL2600 at University of Toledo taught by Williams,F in Fall 2015. Since its upload, it has received 28 views. For similar materials see Funct Anat and Pathophysiol I in Pharmaceutical Sciences at University of Toledo.
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Date Created: 10/06/15
Anatomy Lecture 12 What does a cell do to adapt o Hyperplasia this is an increase of total cell number and not necessarily increase in cell size still leads to enlargement of tissue or organ 0 This can only happen in mitotic cells and that leaves out skeletal cardiac muscle and neurons 0 What is it due to 0 Hormonal stimulation again the uterus during pregnancy may occur at the same time as hypertrophy 0 Compensation if some cells are removed the remaining cells are capable of regenerating at least part of the structure Liver or Kidney 0 Increased workload if remove one kidney will trigger hyperplasia in the other 0 Metaplasia a replacement of 1 type of cell with another often seen in epithelial or mesenchymal derived cells 0 An adaptive substitution by abnormal differentiation of a precursor stem cell Metaplasia 0 Real common in lungs of smokers Chronic smoker will have the epithelial lining of the lung replaced with different cell type columnar cells gt strati ed squamous ep heHaD These cells are more resistant to the smoke but don t secrete mucus smoker s cough and may have a greater chance of infection This is a reversible reaction its not automatic that cancer will develop However this is one of the precancerous conditions that does transform into lung cancer Dysplasia 0 Not an adaptive process common in epithelia 0 Related to metaplasia and hyperplasia 0 See variations in size shape and developmental organization of cell in tissue see a lot of immature cells 0 Changes are seen in nuclei shape size 0 Premalignant condition gt cancer Seen in epithelium of respiratory tract Seen in cervix lmplicated in both cases as a stage of cancer development 0 Cell injury 0 Occurs when stress reaches limits of what call can do to adapt 0 Signs of injury Membrane damage Swelling of mitochondria Swelling of ER Golgi ribosomes Chromatin clumping Membrane damage 0 Chemical agents and physical agents may make holes in the membrane Cell swelling due to increase intake and no control of intake of water Na Ca etc Leakage of enzymes is possible Leakage of K is possible Leakage of protein is a diagnostic test SGOT serum glutamic oxaloacetic transaminase LDH lactic acid dehydrogenase CK creatine kinase Swelling of mitochondria 0 Due to ion imbalance and resulting water uptake 0 Due to failure of active transport systems NaK ATPase Swelling of ER Golgi ribosomes 0 Formation of quotblebsquot or cell surface pieces of membrane 0 Due to swelling controlled by an increase in anaerobic metabolism and the corresponding decrease in ATP 0 Ribosomes detach from the ER Chromatin clumping o Chromatin condenses and clumps without mitotic activity 0 Due to change in pH lower than threshold necessary for proteins and nucleic acids in chromatin All injury 0 Can be reversible if only transient 0 Can become irreversible if persistent for more than a few hours 0 This results in cell death 0 Cell death 0 2 patterns Necrosis more common occurs usually as result of stressor Apoptosis less common more controlled is programmed happens even to healthy cell populations during development 0 Necrosis Due to ischemia loss of blood supply 02 or chemical injury Severe cell swelling and possible rupture of cell membrane followed by in ammation Breakdown of organelles Protein coagulation cytoplasmic proteins will irreversibly form clumps of protein Usually happens after a few hours of exposure to the stressor Nuclear changes with necrosis Pyknosis nucleus shrinks until it is nothing more than a blob of tightly packed chromatin Karyolysis chromatin disappears due to digestion by Dnases from ruptures lysosomes Karyorrhexis nucleus breaks into cumps and is extruded through the cell membrane 0 Apoptosis Regulated event Can occur in normal cells during embryo development Regulates number of cells in tissues Can eliminate potentially dangerous cancer cells Chief features are Chromatin is condensed and fragmented into small dense masses Masses greater near nuclear membrane and extruded karyorrhexis Apoptosis bodies residues of organelles chie y form and are extruded Abnormal cell growth 0 2types Nonneoplasia controlled or reversible usually occurs because of a stimulus stops when stimulus is removed hyperplasia metaplasia dyspasia Neoplasia irreversible uncontrolled persists even after stimulus is gone competes with normal cells for nutrients steadily increases numbers regardless 0 Characteristics of neoplasms Benign Closely resembles normal tissues 0 Slow progressive growth will stop 0 Usually encapsulated and is located 0 Does not metastasize Malignant Anaplasia often does not resemble normal Ussue Could be slow or fast invades tissue Nonencapsulated and invasive Frequently does metastasize
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