Chapter 4 & 6 Cellular Tissue Biology PDF

CHAPTER 4 ALTERED CELLULAR TISSUE BIOLOGY CELLULAR ADAPTATION ↳reversible response to physiologic (normal and pathologic (adverse) changes ADAPTIVE CHANGES ↓Atrophy: gets...

CHAPTER 4 ALTERED CELLULAR TISSUE BIOLOGY CELLULAR ADAPTATION ↳reversible response to physiologic (normal and pathologic (adverse) changes ADAPTIVE CHANGES ↓Atrophy: gets smaller ↳ Hypertrophy: gets bigger - Hyperplasia: higher # in cells * Dysplasia: abnormal changes in size , shape, organization of mature cells, it is irreversible ↳ Metaplasia:reversible replacement of one mature cell type by another ATROPHY HYPERTROPHY HYPERPLASIA DYSPLASIA - PHYSIOLOGIC PATHOLOGIC PHYSIOLOGIC PATHOLOGIC PHYSIOLOGIC PATHOLOGIC * may be reversible results from Dresults from results from if Dnormal in increased Denables Hormonal Stimulus triggering chronic hemodynamic is removed organsto abnorma decrease in early develop. - demand, workload, stimulation by overload blood supply, hormones,growth of cells Dtissues appear disorderly Dhormonal - IT IS NOT CANCER nutrition - factors organs that METAPLASIA respond to endocrine # associated w/ issue damage, repair, regeneration A of stem cells reprogramming or CELLULAR INJURY undifferentiated mesenchymal cells & occurs if cell is unable to maintain homeostasis & reversible: cells recover * irreversible: cells die HYPOXIC INTURY *most common cause of cellular injury RESULTS FROM of blood >ischemia : reduced supply - > loss of - >↓ - hemoglobin production of RBC > diseases in the - respiratory + cardiovascular > poisoning of the oxidative enzumes - ISCHEMIA-REPERFUSION INTURY # cell injury/death caused by restoration of blood flow oxygen Mechanisms > Oxidative stress - > inflammation - > - complement activation > increased intracellular calcium - FREE RADICALS * cause oxidative stress electricallyuncharged atom or group of atoms wh an un paired electron ↑ that damage > lipid peroxidation - > protein alteration - - DNA damage - mitochondrial effects > XENOBIOTICS , carcinogenic, *toxic mutagenic u mercury ⑪ ethano & carbon monoxide ↳ Street drugs * lead * carbon tetrachloride  CELLULAR DEATH *necrosis is the most common and we see it with injury necrosis or apoptosis *there are 5-1 differenttypes of necrosis NECROSIS # rapid loss of plasma membrane , organelleswelling mitochondrial dysfunction , 1. COAGULATIVE NECROSIS * the protein that is found in the cell changes *this can happen in the heart (infarction). LIQUEFACTIVE 2 NECROSIS found in the brain * most commonly nervous systems *occurs to neurons glial cells * bacterial infections in the brain will lead to this. CASEOUS NECROSIS 3 * results from pulmonary tuberculosis infection * after the cells die, they change to a cheese crumbl form 4..FATTY NECROSIS * this will affect more or less the parts of the body that have more fat * tissue becomes Opaque , it is not seethrough , it is chalky white J CANGRENOUS NECROSIS. * death of Tissue from severe hypoxic injury * after the cells die, they change color Example : diabetic persons leg turns purple black swollen , , leg needs to be amputated , APOPTOSIS I 1 *independent cells around the body that shut daun/die * cells are programed to do this when infected * do not die in a , not group a lot of inflammation sign that is protecting itself a our body + aging PHUSIOLOGIC PATHOLOGIC Das a person is growing # not because you are and some cells need aging , but because there is a disease to die for others to live  CHAPTER L Innate Immunity : - Wound Inflammation Healing WHITE BLOOD CELLS - fastest cell * Eneutrophils ↳eosinophils pages - * involved in inflammation * basophils ↓/ lymphocytes L a form of injury *A monocyte have their own form of immunity which is adaptive immunity (vaccines) IMMUNITY 1st line of defense · Innate Immunity >physical mechanical biochemical barriers - , , In 2nd line of defense · Inflammation #3rd line of defense · adaptive (acquired) (specific) immunity # FIRST LINE OF DEFENSE SECOND LINE OF DEFENSE PHYSICAL BARRIERS INFLAMMATORY RESPONSE *body's response to external/internal Skin changes CELL DERIVED CHEMICAL BARRIERS * can be destructive , earwax ↳ tears , saliva , sweat, mucus nonspecific NORMAL MICROBIOME VASCULAR RESPONSE ↓ the surface that is colonized w/ bacteria # can happen because of vasolidation, B fungus and is very particular for the person in they become the location bigger because of the gaps to , platelets M space allows WBC to rescue do clotting PROTECTIVE FUNCTIONS I ⑭prepare for healing/repair PLASMA PROTEIN SYSTEMS # limity control the inflammatory process * essential for effective inflammatory asImplement System kinn resp lotting System System COMPLEMENT SYSTEM I small bits and pieces of protein , biologically active fragments, not cells nor chemicals proteins that have a letter 3 , Oxinizations attraction : C3 and CJ - osponins & C3-ca involved in swelling - chemotactic factors > > anaphylotoxins - - > can caused reaction in body CLOTTING forms a fibrinos meshwork of fibrin Strands and platelets KINIn SYSTEM In cause dilation of blood vessels ⑪important for pain CELLULAR COMPONENTS FUNCTIONS to be WBC -kin microorganisms m mostly going cellular debris & remove of * respond to molecules and are recruited at site damage ↓ activate healing * confine extent of damage CYTOKINES ↓ responsible for activating other cells regulating inflammatory response # cytokines/chemokine chemicals involved in cell : INTERLEUKINS * produced by macrophages and lymphocytes in response to Stimulation of PRRs or by other cytokines INTERFERONS ↑ protects against viral infections Type I produced in the body · : their job is Type 2: only produced by lymphocutes · to activate macrophages increase capacity to detect & process abnormal cells MAST CELLS *the QUEEN# produces a lot of chemicals that are needed for inflammatory response HISTAMINE most important chemical that goes out there 3 causes blood vessels to dilate PHAGOCYTOSIS # a cell that eats