Phys & Patho PDF

PHYA 501 PA FOUNDATIONS II PHYSIOLOGY & PATHOPHYSIOLOGY MARY MINTO, MHS, PA-C UNIVERSITY OF SAINT JOSEPH  WHY ARE WE TALKING ABOUT CELLS IN PA SCHOOL????? FUNCTIONS OF CELLS MOVEMENT...

PHYA 501 PA FOUNDATIONS II PHYSIOLOGY & PATHOPHYSIOLOGY MARY MINTO, MHS, PA-C UNIVERSITY OF SAINT JOSEPH  WHY ARE WE TALKING ABOUT CELLS IN PA SCHOOL????? FUNCTIONS OF CELLS MOVEMENT CONDUCTIVITY SIGNIFICANCE OF CELLS METABOLIC ABSORPTION ALL BODY FUNCTIONS DEPEND ON THE SECRETION INTEGRITY OF THE CELLS EXCRETION UNDERSTANDING CELLULAR BIOLOGY IS RESPIRATION NECESSARY TO UNDERSTAND DISEASE REPRODUCTION COMMUNICATION: “CELLULAR CROSSTALK” IS AT THE HEART OF CELLULAR BIOLOGY BACK TO THE BASICS PROKARYOTES EUKARYOTES NUCLEUS (SINGLE, CIRCULAR COMPLEX CELLULAR ORGANIZATION CHROMOSOME ) MEMBRANE-BOUND ORGANELLES CYANOBACTERIA, BACTERIA, AND WELL-DEFINED NUCLEUS RICKETTSIAE HIGHER ANIMALS, PLANTS, FUNGI, AND PROTOZOA BASIC CELLULAR COMPONENTS- IDENTIFY AND DESCRIBE THEIR FUNCTION PLASMA MEMBRANES- FUNCTION ENCLOSE THE CELL CONTROL THE COMPOSITION OF THE SPACE OR COMPARTMENT THEY ENCLOSE CREATES A BARRIER MAINTAINS POLARITY WITH SELECTIVE TRANSPORT SYSTEM. PROVIDE CELL-TO-CELL RECOGNITION ALLOW FOR CELL-TO-CELL ADHESION PROVIDE CELLULAR MOBILITY AND SHAPE FUNCTION LIKE THE “MOLECULAR GLUE” FOR A CELL AND ORGANELLES PLASMA MEMBRANES- COMPOSITION BILAYER OF LIPIDS AND PROTEINS NOT UNIFORMLY DISTRIBUTED CAN SEPARATE INTO DISCRETE UNITS CALLED MICRODOMAINS AREAS WITHIN THE SAME PLASMA MEMBRANE THAT DIFFER IN PROTEIN AND LIPID COMPOSITION CAVEOLAE CAVE-LIKE INDENTATIONS FUNCTIONS: STORAGE AREA FOR RECEPTOR, ROUTE FOR TRANSPORT INTO CELL, AND ACT AS THE INITIATOR FOR RELAYING INFO FROM EXTRACELLULAR CHEMICAL MESSENGERS INTO THE CELL PLASMA MEMBRANES- COMPOSITION LIPIDS SOLID-GEL PHASE; FLUID-LIQUID CRYSTALLINE PHASE; LIQUID-ORDERED PHASE PHASES CAN CHANGE IN RESPONSE TO TEMPERATURE AND PRESSURE AMPHIPATHIC LIPIDS HYDROPHILIC AND HYDROPHOBIC ENDS OF EACH LIPID MOLECULE = LIPID BILAYER CONTROL MOVEMENT OF HYDROPHILIC SUBSTANCES AND WATER ALLOW LIPOPHILIC SUBSTANCES TO MOVE FREELY (OXYGEN AND CO 2)  PLASMA MEMBRANES- COMPOSITION PROTEINS ARE MADE FROM A CHAIN OF AMINO ACIDS KNOWN AS POLYPEPTIDES PROTEINS ARE THE MAJOR “WORKHORSES” OF THE CELL. POSTTRANSLATIONAL MODIFICATIONS PLAY A ROLE IN DISEASE DEVELOPMENT FUNCTIONS MADE BY RIBOSOMES AND TRAVEL TO RECEPTORS VARIOUS LOCATIONS IN THE MEMBRANES TRANSPORTERS (TRAFFICKING) ENZYMES INVOLVES FOLDING AND UNFOLDING AND MOVING THE PROTEINS WHICH CAN LEND SURFACE MARKERS ITSELF TO ERRORS = DISEASE ADHESION MOLECULES INCLUDE INTEGRAL, PERIPHERAL, AND CATALYSTS TRANSMEMBRANE CELL-ADHESION MOLECULES (INTEGRINS, CADHERINS, SELECTINS, AND IMMUNOGLOBULIN SUPERFAMILY CAM S) PLASMA MEMBRANE PROTEINS CELLULAR RECEPTORS PROTEIN MOLECULES ON THE PLASMA MEMBRANE, CYTOPLASM, OR NUCLEUS USUALLY ATTACHED TO INTEGRAL PROTEINS PROTEINS THAT BIND WITH LIGANDS (SMALLER MOLECULES) THAT “FIT” THE SHAPE OF THE RECEPTOR LIGANDS= HORMONES, NEUROTRANSMITTERS, ANTIGENS, COMPLEMENT COMPONENTS, INFECTIOUS AGENTS, DRUGS, ETC PLASMA MEMBRANE RECEPTORS: DETERMINE WITH WHICH LIGANDS A CELL WILL BIND (MUST FIT TOGETHER) DETERMINE HOW THE CELL WILL RESPOND TO THE BINDING MAY OPEN AN ION CHANNEL MAY INITIATE AN INTERACTION, CAUSING ADENYLYL CYCLASE TO TRANSFORM ADENOSINE TRIPHOSPHATE (ATP) TO MESSENGER MOLECULES THAT STIMULATE SPECIFIC RESPONSES IN THE CELL PLASMA MEMBRANES- COMPOSITION PROTEASES ARE ENZYMES THAT ARE TETHERED TO THE CELL MEMBRANE INVOLVED IN THE PROTEOLYTIC CASCADE TIGHTLY ORCHESTRATED SEQUENCE OF EVENTS THAT CAUSE THE BREAKDOWN OF PROTEIN FOR PURPOSES OF PHYSIOLOGIC REGULATION MAY ACT AS INITIATOR OR HELP WITH AMPLIFICATION AND PROPAGATION OR EXECUTION FOUR MAJOR CASCADES CASPASE-MEDIATED APOPTOSIS (CELL DEATH) BLOOD COAGULATION CASCADE MATRIX METALLOPROTEINASE CASCADE COMPLEMENT CASCADE DRUG INTERVENTIONS ARE BASED ON THE ACTION OF THESE PROTEASES ABNORMAL FUNCTION OF THE PROTEASES IS IMPORTANT IN DEVELOPMENT OF VARIOUS DISEASE (CANCER, AUTOIMMUNITY, AND NEURODEGENERATIVE DISORDERS) PLASMA MEMBRANES- COMPOSITION CARBOHYDRATES (OLIGOSACCHARIDES) ARE CONTAINED WITHIN THE PLASMA MEMBRANE BOUND TO MEMBRANE PROTEINS AND LIPIDS FUNCTION IN INTERCELLULAR RECOGNITION (REQUIRED FOR TISSUE FORMATIONS) ABNORMAL SURFACE CARBOHYDRATE MARKERS ARE IMPLICATED IN TUMOR CELLS EXTRACELLULAR MATRIX MESHWORK OF FIBROUS PROTEINS EMBEDDED IN WATER, GEL-LIKE CARBOHYDRATES SECRETED FROM CELLS TO ENVELOPE THEMSELVES INCLUDES MACROMOLECULES AND BASAL LAMINA FUNCTIONS “GLUES” CELLS TOGETHER PATHWAY FOR DIFFUSION OF NUTRIENTS, WATS, AND OTHER WATER-SOLUBLE THINGS THROUGH THE BLOOD AND TISSUE CELLS INVOLVED IN REGULATING CELL BEHAVIORS https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved =0ahUKEwjZ15uqsa3YAhVscd8KHc6QAfQQjRwIBw&url=https%3A%2F%2Fwww.khanacademy.org% 2Fscience%2Fbiology%2Fstructure-of-a-cell%2Fcytoskeleton-junctions-and-extracellular- structures%2Fa%2Fthe-extracellular-matrix-and-cell- wall&psig=AOvVaw3p0TwwSF9EBEbAuBSgkcFT&ust=1514573825516762  CELL JUNCTIONS SPECIALIZED AREAS OF THE CELL MEMBRANES (3 TYPES) = JUNCTIONAL COMPLEX DESMOSOMES (ADHERING JUNCTIONS) TIGHT JUNCTIONS (IMPERMEABLE JUNCTIONS) GAP JUNCTIONS(COMMUNICATING JUNCTIONS) FUNCTION: HOLD CELLS TOGETHER ALLOW MOVEMENT OF SMALL MOLECULES FROM CELL TO CELL PERMEABILITY OF THE JUNCTIONAL COMPLEX IS REGULATED BY GATING (DEPENDENT ON CALCIUM CONCENTRATION )  CYTOPLASM FILLS THE SPACE BETWEEN THE NUCLEUS AND THE FUNCTIONS PLASMA MEMBRANE SYNTHESIS AND TRANSPORT ELIMINATES WASTES STRUCTURE METABOLIC PROCESSES CYTOPLASMIC MATRIX MAINTENANCE CYTOSOL MOTILITY CYTOPLASMIC ORGANELLES STORAGE CYTOPLASMIC/INTRACELLULAR ORGANELLES CYTOSOL STRUCTURE GELATINOUS, SEMILIQUID PORTION OF THE CYTOPLASM 55% OF THE TOTAL CELL VOLUME FUNCTIONS INTERMEDIARY METABOLISM INVOLVING ENZYMATIC BIOCHEMICAL REACTIONS RIBOSOMAL PROTEIN SYNTHESIS STORAGE  CYTOPLASMIC/INTRACELLULAR ORGANELLES CYTOSKELETON “BONES AND MUSCLES” OF THE CELL MAINTAINS THE CELL’S SHAPE AND INTERNAL ORGANIZATION PERMITS MOVEMENT OF SUBSTANCES WITHIN THE CELL AND MOVEMENT OF EXTERNAL PROJECTIONS INTERNAL SKELETON = MICROTUBULES AND MICROFILAMENTS MICROTUBULES CENTRIOLES MICROFILAMENTS: ACTIN CELL TO CELL JUNCTIONS MECHANOTRANSDUCTION INTRACELLULAR ORGANELLES RIBOSOMES STRUCTURE: RIBONUCLEIC ACID (RNA) PROTEIN COMPLEXES MADE AND SECRETED BY THE NUCLEUS FREE VS. ATTACHED RIBOSOMES FUNCTION: SYNTHESIZE PROTEINS ENDOPLASMIC RETICULUM STRUCTURE: NETWORK OF TUBULAR OR SACLIKE CHANNELS SMOOTH VS. ROUGH ENDOPLASMIC RETICULUM FUNCTION: SITE OF PROTEIN SYNTHESIS SENSES CELLULAR STRESS AND MAY RESPOND WITH “MISFOLDING” OF PROTEINS  INTRACELLULAR ORGANELLES GOLGI COMPLEX STRUCTURE FLATTENED, SMOOTH MEMBRANES LOCATED NEAR NUCLEUS RECEIVES PROTEINS FROM THE ER (TRANSPORT VESICLES CONGREGATE AT THE CISTERNAE OF THE GOLGI APPARATUS) FUNCTIONS “REFINING PLANT” AND DIRECTS TRAFFIC PROCESSES, SECRETES, AND RELEASES SUBSTANCES (PROTEINS, LIPIDS, ENZYMES, POLYSACCHARIDES) SUBSTANCES PACKAGED IN GOLGI COMPLEX INTO CLATHRIN-COATED VESICLES INTRACELLULAR ORGANELLES LYSOSOMES STRUCTURE SACLIKE STRUCTURES THAT ORIGINATE FROM THE GOLGI PRIMARY LYSOSOMES = RESTING SECONDARY LYSOSOMES = ACTIVE, VERY ACIDIC, BOUND TO VESICLE AUTOLYSOSOMES = DIGEST DEBRIS FUNCTIONS INTRACELLULAR DIGESTION SYSTEM HYDROLASES: 40 DIGESTIVE ENZYMES ROLE IN AUTODIGESTION AND AUTOPHAGY RESIDUAL BODIES GET EXPELLED FROM VACUOLE = PRODUCTS THAT CANNOT BE DIGESTED INTRACELLULAR ORGANELLES PEROXISOMES STRUCTURE MEMBRANE-BOUND ORGANELLES THAT CONTAIN OXIDATIVE ENZYME CATALASE AND URATE OXIDASE FUNCTIONS ARE THE MAJOR SITES OF OXYGEN UTILIZATION DETOXIFY COMPOUNDS AND FATTY ACIDS BY USING H2O2 THAT IS STORED IN THE ORGANELLE AND BREAKING DOWN SUBSTANCES INTO HARMLESS PRODUCTS PHENOLS, FORMIC ACID, FORMALDEHYDE, ALCOHOL SYNTHESIZE SPECIALIZED PHOSPHOLIPIDS FOR NERVE CELL MYELINATION.  INTRACELLULAR ORGANELLES MITOCHONDRIA STRUCTURE IS SURROUNDED BY A DOUBLE MEMBRANE OUTER MEMBRANE: SMOOTH, PERMEABLE INNER MEMBRANE: VERY SELECTIVE, CONTAINS ENZYMES FOR OXIDATIVE PHOSPHORYLATION CRISTAE INCREASE SURFACE AREA MATRIX: INNER PORTION OF ORGANELLE, INVOLVED IN METABOLISM FUNCTIONS RESPONSIBLE FOR CELLULAR RESPIRATION AND ENERGY PRODUCTION PARTICIPATES IN OXIDATIVE PHOSPHORYLATION NEWER RESEARCH SUGGESTS MITOCHONDRIA HAVE A ROLE IN DETERMINING CELL DEATH (RELEASE OF CYTOCHROME C) INTRACELLULAR ORGANELLES VAULTS (AKA RIBONUCLEOPROTEINS) STRUCTURE BIGGER THAN RIBOSOMES, SHAPED AS OCTAGONAL BARRELS THOUSANDS PRESENT IN CELL FUNCTION HYPOTHESIZED TO BE THE CELL’S “TRUCK” THAT CARRY MESSENGER RNA (MRNA) FROM THE NUCLEUS TO THE RIBOSOMES NUCLEAR ENVELOPE HAS SIMILARLY SHAPED PORES INTRACELLULAR ORGANELLES NUCLEUS STRUCTURE NUCLEAR ENVELOPE NUCLEOLUS DEOXYRIBONUCLEIC ACID (DNA) DNA REPLICATION, REPAIR, AND TRANSCRIPTION HISTONE PROTEINS FUNCTIONS CELL DIVISION AND CONTROL OF GENETIC INFORMATION DNA REPAIR AND TRANSCRIPTION  DESCRIBE AND DIFFERENTIATE THE CELLULAR METHODS OF TRANSPORT AND COMMUNICATION  CELLULAR METHODS OF COMMUNICATION COMMUNICATION BETWEEN CELLS IS REQUIRED TO MAINTAIN HOMEOSTASIS, REGULATE GROWTH AND DIVISION, AND COORDINATE CELL FUNCTION 3 MAIN WAYS TO COMMUNICATE SIGNAL MOLECULE BINDS TO A PLASMA MEMBRANE RECEPTOR SIGNAL MOLECULE ENTERS THE CELL AND BINDS TO RECEPTOR PROTEINS INSIDE THE TARGET CELL CELLS CONNECT VIA PROTEIN CHANNELS (GAP JUNCTIONS) AND DIRECTLY COORDINATE ACTIVITIES CATEGORIZING CELLULAR COMMUNICATION SIGNAL TRANSDUCTION WHAT HAPPENS AFTER THE SIGNALLING CELL SENDS ITS MESSAGE TO THE TARGET CELL(S)?? MESSAGE IS USED TO CONVEY INSTRUCTIONS TO THE CELL’S INTERIOR ORGANELLES: TRANSFER, AMPLIFY, DISTRIBUTE, OR MODULATE HOW? THE LIGAND (EXTRACELLULAR SIGNALING MESSENGER = 1ST MESSENGER) BINDS THEN HAS TWO OPTIONS FOR AFFECTING THE TARGET CELL OPENS OR CLOSES CHANNELS TO REGULATE MOVEMENT OF ION IT TRANSFERS THE SIGNAL TO AN INTRACELLULAR MESSENGER (SECOND MESSENGER) WHICH THEN CAUSES A BUNCH OF EVENTS IN THE CELL TWO OPTIONS FOR 2ND MESSENGER SYSTEM CAMP CA2+ SIGNAL TRANSDUCTION CELLULAR TRANSPORT WHAT IS BEING MOVED AND WHERE? SOLUTES = DISSOLVED STUFF ELECTROLYTES (CATION (+) OR ANIONS (–)) MEASURED IN MILLIEQUIVALENTS PER LITER (MEQ/L) OR MILLIGRAMS PER DECILITER (MG/DL) NONELECTROLYTES EXAMPLES: OXYGEN, CARBON DIOXIDE, GLUCOSE, UREA, AND CREATININE DO NOT DISSOCIATE WHEN PLACED IN SOLUTION MOVING IN AND OUT OF CELL CELLULAR METHODS OF TRANSPORT- PASSIVE TRANSPORT OCCURS WHEN WATER AND SMALL, ELECTRICALLY UNCHARGED MOLECULES MOVE THROUGH PORES DOES NOT REQUIRE ENERGY TYPES OF PASSIVE TRANSPORT DIFFUSION PASSIVE MEDIATED TRANSPORT = FACILITATED DIFFUSION FILTRATION: HYDROSTATIC PRESSURE  PASSIVE TRANSPORT- DIFFUSION SOLUTE MOVES FROM AREA OF GREATER CONCENTRATION TO ONE OF LESSER CONCENTRATION ELECTRICAL CHARGE SIZE LIPID SOLUBILITY  PASSIVE TRANSPORT- HYDROSTATIC & ONCOTIC PRESSURES FILTRATION = MOVEMENT OF WATER/SOLUTES THROUGH MEMBRANE B/C OF A PUSHING FORCE PUSHING FORCE = HYDROSTATIC PRESSURE OSMOSIS = MOVEMENT OF WATER FROM LOTS OF WATER TO AREAS WITH LESS WATER PULLING FORCE = COLLOID OSMOTIC PRESSURE (ONCOTIC PRESSURE) TONICITY = OSMOLALITY OF SOLUTION = CONCENTRATION OF MOLECULES PER WEIGHT OF WATER MEDIATED TRANSPORT INTEGRAL PROTEINS ALLOW MOVEMENT OF INORGANIC ANIONS, CATIONS, AND LARGE, UNCHARGED COMPOUNDS ACROSS THE MEMBRANE BINDING OF A SPECIFIC SOLUTE → CONFORMATIONAL CHANGE IN PROTEIN → ALLOWS SOLUTE TO CROSS CELL MEMBRANE ACTIVE OR PASSIVE TRANSPORT PASSIVE MEDIATED TRANSPORT = FACILITATED DIFFUSION = NO ENERGY NEEDED MOLECULES MOVE DOWN CONCENTRATION GRADIENT ACTIVE MEDIATED TRANSPORT = ACTIVATED TRANSPORT MEDIATED TRANSPORT TRANSPORT/CARRIER PROTEIN CHANNEL PROTEIN/ION CHANNEL MEDIATED TRANSPORT UNIPORT = MOVING ONE MOLECULE SYMPORT = MOVING 2 MOLECULES IN THE SAME DIRECTION AT THE SAME TIME ANTIPORT = MOVING 2 MOLECULES IN OPPOSITE DIRECTIONS AT THE SAME TIME  CELLULAR METHODS OF TRANSPORT- ACTIVE MEDIATED TRANSPORT ACTIVE MEDIATED TRANSPORT (TRANSPORTER PROTEIN) REQUIRES THE EXPENDITURE OF ENERGY- USUALLY ATP MOVES MOLECULES AGAINST A CONCENTRATION GRADIENT LARGER MOLECULES AND MOLECULAR COMPLEXES (E.G., LIGAND-RECEPTOR COMPLEXES) ARE MOVED INTO THE CELL. ONE EXAMPLE OF AN ACTIVE TRANSPORT PUMP IS ION CHANNELS WITH CARRIER. POTASSIUM-SODIUM ANTIPORT SYSTEM NA+ MOVES OUT WHEN K+ MOVES INTO THE CELL WHEN THE TRANSPORTER PROTEIN (ACTUALLY AN ENZYME CALLED ATPASE) GETS FUEL (ATP) TO WORK 3 NA+ MOVE OUT FOR EVERY 2 K+ THAT MOVE IN = ESTABLISHES AN ELECTRICAL POTENTIAL (INSIDE IS MORE NEGATIVE THAN THE OUTSIDE OF THE CELL) THAT IS CRUCIAL TO THE BODY ACTIVE TRANSPORT TRANSPORT BY VESICLE FORMATION ENDOCYTOSIS—TAKING IN INTERNALIZING PROCESS: SECTION OF PLASMA MEMBRANE ENFOLDS SUBSTANCES FROM OUTSIDE THE CELL; THEN INVAGINATES AND SEPARATES FROM THE PLASMA MEMBRANE, FORMING A VESICLE THAT MOVES INSIDE THE CELL PINOCYTOSIS: CELL INGESTION OF ECF AND ITS CONTENTS OCCURS. PHAGOCYTOSIS: LARGE MOLECULAR SUBSTANCES ARE ENGULFED BY THE PLASMA MEMBRANE AND ENTER THE CELL SO THAT THESE SUBSTANCES CAN BE ISOLATED AND DESTROYED BY LYSOSOMAL ENZYMES EXOCYTOSIS—EXPELLING DISCHARGE OR SECRETION OF MATERIAL FROM THE INTRACELLULAR VESICLES AT THE CELL SURFACE MAY BE EXPELLED INTO THE EXTRACELLULAR MATRIX OR MAY ADHERE TO THE PLASMA MEMBRANE (REPLACEMENT OF AREAS OF THE MEMBRANE THAT WERE LOST TO ENDOCYTOSIS) ENDOCYTOSIS AND EXOCYTOSIS TRANSPORT OF ELECTRICAL IMPULSES RESTING MEMBRANE POTENTIAL: DIFFERENCE IN VOLTAGE ACROSS THE PLASMA MEMBRANE ALL BODY CELLS ARE ELECTRICALLY POLARIZED INSIDE OF THE CELL IS MORE NEGATIVELY CHARGED THAN THE OUTSIDE ESTABLISHED THROUGH MOVEMENT OF IONS ACROSS CELL MEMBRANE ACTION POTENTIALS ARE AN EXAMPLE OF HOW ELECTRICAL IMPULSES ARE TRANSPORTED THROUGH THE BODY MOVEMENT OF IONS → CONFORMATIONAL CHANGES IN OTHER MEMBRANE PROTEINS → MORE MOVEMENT OF IONS; REPEAT = MESSAGE BEING CARRIED THROUGH BODY END ORGAN ALSO HAS CHANGES IN SOLUTE MOVEMENT → SOME ACTION BEING PERFORMED BY THE CELL  DESCRIBE THE COMPOSITION AND FUNCTION OF THE PRIMARY TYPES OF TISSUES IN THE BODY PRIMARY TYPES OF TISSUES IN THE BODY CELLS WITH COMMON STRUCTURE AND FUNCTION ARE ORGANIZED INTO TISSUES (4 TYPES) EPITHELIAL CONNECTIVE MUSCLE NEURAL FOUNDER CELLS CHEMOTAXIS CONTACT GUIDANCE STEM CELLS SELF RENEWAL MULTIPOTENCY TISSUE FORMATION MITOSIS OF FOUNDER CELLS (MOST BASIC PRECURSOR CELLS) HELD IN PLACE BY SPECIALIZED JUNCTIONS ON THEIR PLASMA MEMBRANES AND BY MACROMOLECULES IN THE ECM Epithelial cell MAY FORM SHEETS (EXAMPLE= EPITHELIAL sheet CELL SHEETS) TISSUE FORMATION MIGRATION OF SPECIALIZED CELLS FOLLOWED BY ASSEMBLY AT THE SITE OF TISSUE FORMATION HOW DO THE CELLS KNOW WHERE TO MIGRATE TO? CHEMOTAXIS = MOVEMENT ALONG A CHEMICAL GRADIENT (CELLS AT THE DESTINATION SITE SECRETE A CHEMOTACTIC FACTOR THAT ATTRACTS SPECIFIC CELLS) CONTACT GUIDANCE = MOVEMENT OF CELLS ALONG A PATHWAY WITHIN THE EXTRACELLULAR MATRIX EXAMPLE: NEURAL CREST CELLS MIGRATE TO DIFFERENT AREAS WHERE THEY FORM A VARIETY OF TISSUES LIKE THE PERIPHERAL NERVOUS SYSTEM TISSUE FORMATION STEM CELLS CELLS THAT CAN DEVELOP INTO MANY DIFFERENT CELL TYPES EARLY IN THEIR DEVELOPMENT AND GROWTH (MULTIPOTENT) DIFFERENTIATION CAN SERVE AS INTERNAL REPAIR AND MAINTENANCE SYSTEM EXAMPLES: EPITHELIAL LINING OF THE INTESTINE , STOMACH, AND SKIN  EPITHELIAL TISSUE COVERS MOST INTERNAL AND EXTERNAL BODY SURFACES CATEGORIZED BY NUMBER AN ARRANGEMENT OF CELL LAYERS SIMPLE VS. STRATIFIED VS. PSEUDOSTRATIFIED CATEGORIZED BY CELL SHAPE SQUAMOUS, CUBOIDAL, COLUMNAR, PSEUDOSTRATIFIED STRUCTURE VARIES BASED ON LOCATION AND FUNCTION CILIA AND MICROVILLI FUNCTIONS PROTECTION, ABSORPTION, SECRETION, AND EXCRETION  CONNECTIVE TISSUE STRUCTURE FUNCTION VARIES ABUNDANT EXTRACELLULAR MATRIX FRAMEWORK FOR FORMING ORGANS SURROUNDING A FEW CELLS BINDING TISSUES AND ORGANS TOGETHER GROUND SUBSTANCE SUPPORTING TISSUES AND ORGANS IN THEIR FIBERS LOCATIONS COLLAGENOUS (WHITE), ELASTIC (YELLOW), AND RETICULAR STORING EXCESS NUTRIENTS LOOSE AND DENSE CONNECTIVE TISSUE MUSCLE TISSUE STRUCTURE COMPOSED OF MYOCYTES (LONG, THIN CELLS) 3 KINDS OF MUSCLE TISSUE: SMOOTH, SKELETAL, AND CARDIAC FUNCTIONS CONTRACTION- ENABLING BOTH VOLUNTARY AND INVOLUNTARY MOVEMENT NEURAL TISSUE STRUCTURE COMPOSED OF SPECIALIZED CELLS CALLED NEURONS WHICH CAN VARY IN APPEARANCE ALL NEURONS HAVE: SYNAPSES, CELL BODIES, AXONS (MESSAGE AWAY FROM CELL), AND DENDRITES (MESSAGE TO THE CELLS) FUNCTIONS RECEIVE AND TRANSMIT ELECTRICAL IMPULSES VERY RAPIDLY ACROSS JUNCTIONS CALLED SYNAPSES NEUROTRANSMITTERS (CHEMICAL MESSENGERS) DIFFERENTIATE THE FUNCTIONS AND ACTIONS OF THE SYMPATHETIC AND PARASYMPATHETIC SYSTEMS  NERVOUS SYSTEM CNS PNS BRAIN SPINAL CORD EVERYTHING ELSE (MOTOR & SENSORY NEURONS, GANGLIA) AUTONOMIC NS SOMATIC NS SYMPATHETIC NS PARASYMPATHETIC NS AUTONOMIC NERVOUS SYSTEM COORDINATES AND MAINTAINS A STEADY-STATE AMONG VISCERAL ORGANS (CARDIAC MUSCLE, SMOOTH MUSCLE, AND GLANDS IN THE BODY) INVOLUNTARY SYSTEM DIFFERENT FROM SOMATIC NERVOUS SYSTEM B/C MOTOR COMPONENT IS A TWO NEURON SYSTEM: PREGANGLIONIC (MYELINATED) NEURONS AND POSTGANGLIONIC (UNMYELINATED) NEURONS FUNCTIONALLY SPLIT INTO 2 DIVISIONS: SYMPATHETIC NERVOUS SYSTEM PARASYMPATHETIC NERVOUS SYSTEM SYMPATHETIC NERVOUS SYSTEM (ANS) FUNCTION IS TO MOBILIZE ENERGY STORES WHEN REQUIRED (FIGHT OR FLIGHT RESPONSE) GETS INFO FROM CELL BODIES T1- L2(ISH) CELL BODIES PREGANGLIONIC NEURONS RELEASE ACH (BINDS TO NICOTINIC RECEPTORS) POSTGANGLIONIC NEURONS RELEASE NOREPINEPHRINE SOME CHOLINERGIC RELEASE TO SWEAT GLANDS PARASYMPATHETIC NERVOUS SYSTEM (ANS) FUNCTION IS TO CONSERVE AND RESTORE ENERGY: BRADYCARDIA, BRONCHIOLAR /PUPILLARY CONSTRICTION, INCREASED SECRETIONS AND PERISTALSIS CELL BODIES LOCATED IN THE CRANIAL NERVE NUCLEI AND SACRAL SPINAL CORD LONG PREGANGLIONIC NEURONS, SHORT POSTGANGLIONIC NEURONS ACETYLCHOLINE RELEASED FROM PRE AND POST GANGLIONIC NEURONS PATHOPHYSIOLOGY CELLULAR ADAPTATION REVERSIBLE, STRUCTURAL OR FUNCTIONAL RESPONSE TO NORMAL (PHYSIOLOGIC) OR ADVERSE (PATHOLOGIC) CONDITIONS IT’S THE CELL’S RESPONSE TO ESCAPE AND PROTECT ITSELF FROM INJURY OR TO MAINTAIN HOMEOSTASIS AN ADAPTED CELL IS NOT A NORMAL CELL, BUT IT IS NOT AN INJURED CELL EITHER TYPES OF CELLULAR ADAPTATION ATROPHY: DECREASE IN CELL SIZE HYPERTROPHY: INCREASE IN CELL SIZE HYPERPLASIA: INCREASE IN CELL NUMBER METAPLASIA: REVERSIBLE REPLACEMENT OF ONE MATURE CELL TYPE BY ANOTHER LESS MATURE CELL TYPE DYSPLASIA: DERANGED CELLULAR GROWTH; IS NOT A TRUE CELLULAR ADAPTATION BUT RATHER AN ATYPICAL HYPERPLASIA CELLULAR ADAPTATION- ATROPHY PHYSIOLOGIC OCCURS WITH EARLY DEVELOPMENT (THYMUS) PATHOLOGIC RESULTS FROM DECREASES IN WORKLOAD, USE, PRESSURE, BLOOD SUPPLY, NUTRITION, HORMONAL STIMULATION , AND NERVOUS STIMULATION HOW DO THE CELLS BECOME SMALLER? DECREASED PROTEIN SYNTHESIS D/T FEWER MITOCHONDRIA AND LESS ENDOPLASMIC RETICULUM INCREASED PROTEIN CATABOLISM D/T UPREGULATION OF THE UBIQUITIN-PROTEASOME PATHWAY AUTOPHAGY – VACUOLES “DIGEST” THE CELLULAR DEBRIS CELLULAR ADAPTATION- ATROPHY CELLULAR ADAPTATION- HYPERTROPHY CAUSED BY INCREASED WORK DEMAND OR HORMONES TRIGGER SIGNALS: MECHANICAL (STRETCH AND TROPHIC (GROWTH FACTORS AND VASOACTIVE AGENTS) PHYSIOLOGIC HEART ENLARGES TO ACCOMMODATE INCREASED DEMAND AND/OR VOLUME OCCURS IN RESPONSE TO POSTNATAL REQUIREMENTS, MODERATE EXERCISE TRAINING, PREGNANCY , AND EARLY PHASE OF VOLUME/PRESSURE INCREASES PATHOLOGIC LIKELY OCCURS IF THE PHYSIOLOGIC RESPONSE IS PROLONGED (? DEFINITION OF PROLONGED = DEPENDENT ON PERSON) LIKELY RELATED TO RESTRICTION IN MYOCYTE GROWTH (EVENTUALLY DEMAND > ADAPTATION = FAILURE) CELLULAR ADAPTATION- HYPERTROPHY CELLULAR ADAPTATION- HYPERPLASIA CAUSED BY INCREASED RATE OF CELLULAR DIVISION = INCREASED NUMBER OF CELLS OFTEN OCCURS WITH HYPERTROPHY ENLARGED NUCLEUS, CLUMPING OF CHROMATIN, PRESENCE OF ONE OR MORE ENLARGED NUCLEOLI PHYSIOLOGIC COMPENSATORY: ALLOWS ORGANS TO REGENERATE MEDIATED BY DIFFERENT GROWTH FACTORS, CYTOKINES, INTERLEUKINS, AND TUMOR NECROSIS FACTORS NOT AL CELLS ARE CAPABLE OF COMPENSATORY HYPERPLASIA (DEBATE ABOUT NEURONS), BUT SOME ARE GREAT EXAMPLES (LIVER) HORMONAL: REPLACES LOST TISSUE OR SUPPORTS NEW GROWTH EXAMPLE: IMPLANTATION OF FERTILIZED OVUM LEADS TO HORMONAL STIMULATION OF THE UTERUS CAUSING HYPERTROPHY AND HYPERPLASIA AS THE UTERUS GROWS WITH FETUS PATHOLOGIC ABNORMAL PROLIFERATION OF NORMAL CELLS (MAY BE IN RESPONSE TO EXCESS HORMONE STIMULATION OR GROWTH FACTORS) EXAMPLE: ENDOMETRIAL HYPERPLASIA (IMBALANCE BETWEEN ESTROGEN AND PROGESTERONE CELLULAR ADAPTATION- DYSPLASIA & METAPLASIA DYSPLASIA REFERS TO ABNORMAL CHANGES IN THE SIZE, SHAPE, AND ORGANIZATION OF MATURE CELLS. CAN BE CALLED ATYPICAL HYPERPLASIA. DOES NOT INDICATE CANCER. METAPLASIA IS THE REVERSIBLE REPLACEMENT OF ONE MATURE CELL BY ANOTHER LESS MATURE CELL TYPE. REPLACEMENT OF NORMAL BRONCHIAL COLUMNAR CILIATED EPITHELIAL CELLS BY STRATIFIED SQUAMOUS EPITHELIAL CELLS IS A REPROGRAMMING OF STEM CELLS. MECHANISMS OF CELLULAR INJURY AND DEATH DIFFERENTIATE THE VARIOUS PROCESSES CELLULAR INJURY LEADS TO INJURY OF TISSUES AND ORGANS, DETERMINING STRUCTURAL PATTERNS OF DISEASE. INJURED CELLS MAY RECOVER (REVERSIBLE INJURY) OR DIE (IRREVERSIBLE INJURY). CAUSES CELL STRESS. IS ACUTE OR CHRONIC AND REVERSIBLE OR IRREVERSIBLE. CAN INVOLVE NECROSIS, APOPTOSIS, AUTOPHAGY, ACCUMULATION, OR PATHOLOGIC CALCIFICATION. CELLULAR INJURY (CONT’D) INJURY AND RESPONSES  CELLULAR INJURY (CONT’D) CELLULAR INJURY CAN LEAD TO CELL DEATH BY: CAUSES OF CELL INJURY DECREASED ATP PRODUCTION LACK OF OXYGEN (HYPOXIA) FAILURE OF ACTIVE TRANSPORT MECHANISMS (SODIUM- FREE RADICALS POTASSIUM [NA+/K+] PUMP) CELLULAR SWELLING CAUSTIC OR TOXIC CHEMICALS DETACHMENT OF RIBOSOMES FROM ENDOPLASMIC INFECTIOUS AGENTS RETICULUM CESSATION OF PROTEIN SYNTHESIS UNINTENTIONAL AND INTENTIONAL INJURY MITOCHONDRIAL SWELLING FROM CALCIUM INFLAMMATORY AND IMMUNE RESPONSES ACCUMULATION GENETIC FACTORS VACUOLATION LEAKAGE OF DIGESTIVE ENZYMES FROM LYSOSOMES; INSUFFICIENT NUTRIENTS AUTODIGESTION OF INTRACELLULAR STRUCTURES PHYSICAL TRAUMA FROM MANY CAUSES LYSIS OF THE PLASMA MEMBRANE DEATH CELLULAR INJURY (CONT’D) FOUR BIOCHEMICAL THEMES: 1. ADENOSINE TRIPHOSPHATE (ATP) DEPLETION 2. OXYGEN AND OXYGEN-DERIVED FREE RADICALS 3. INTRACELLULAR CALCIUM AND LOSS OF CALCIUM STEADY STATE 4. DEFECTS IN MEMBRANE PERMEABILITY CELLULAR INJURY (CONT’D) HYPOXIC INJURY—LACK OF OXYGEN ISCHEMIA: DECREASED BLOOD FLOW INTO VESSELS THAT SUPPLY THE CELL WITH OXYGEN AND NUTRIENTS ANOXIA: SUDDEN CESSATION OF OXYGEN SUPPLY D/T ACUTE OBSTRUCTION CELLULAR RESPONSES DECREASE IN ATP, CAUSING FAILURE OF THE NA+/K+ PUMP AND SODIUM-CALCIUM EXCHANGE CELLULAR SWELLING CELLULAR INJURY (CONT’D) REPERFUSION INJURY RESTORATION OF OXYGEN LEADS TO FORMATION OF XANTHINE OXIDASE WHILE THE CELL WAS ISCHEMIC (PRIOR TO REPERFUSION), ANAEROBIC METABOLISM WAS CAUSING A BUILD UP OF PURINE CATABOLITES (XANTHINE AND HYPOXANTHINE) RESTORATION OF OXYGEN LEADS TOT FORMATION OF XANTHINE OXIDASE WHICH LEADS TO MASSIVE AMOUNTS OF SUPEROXIDE AND HYDROGEN PEROXIDE BUILD UP THESE CAUSE MEMBRANE DAMAGE AND CALCIUM OVERLOAD WHICH LEAD TO THE OPENING OF THE MITOCHONDRIAL MEMBRANE = MASSIVE ESCAPE OF ATP AND SOLUTES = CELL DEATH  CELLULAR INJURY (CONT’D) FREE RADICALS AND REACTIVE OXYGEN SPECIES (ROS)—OXIDATIVE STRESS FREE RADICALS OR ROS = ELECTRICALLY UNCHARGED ATOM OR GROUP OF ATOMS HAVING AN UNPAIRED ELECTRON RESULTS IN MEMBRANE DAMAGE TYPES OF DAMAGE LIPID PEROXIDATION WHEN CHEMICAL BINDS WITH LIPIDS IN MEMBRANES AND DAMAGES THEM ALTERATION OF PROTEINS AFTER MITOCHONDRIA DAMAGED ALTERATION OF DNA AFTER MITOCHONDRIA DAMAGED MECHANISMS FOR INACTIVATION OF FREE RADICALS MITOCHONDRIAL OXIDATIVE STRESS CELLULAR INJURY (CONT’D) CHEMICAL INJURY DIRECT TOXICITY TO THE CELL DAMAGE TO OR DESTRUCTION OF PLASMA MEMBRANE REACTIVE FREE RADICALS AND LIPID PEROXIDATION EXAMPLES: LEAD CARBON MONOXIDE ETHANOL MERCURY SOCIAL OR STREET DRUGS  CELLULAR INJURY (CONT’D) LEAD CARBON MONOXIDE (CO) MOST COMMON SOURCE IS PAINT IN OLDER PRODUCES HYPOXIC INJURY HOMES (CHILDREN) AND AT WORK (ADULTS) DIRECTLY REDUCES THE OXYGEN- IT IS ABLE TO BIND TO MANY DIFFERENT CARRYING CAPACITY OF BLOOD, AND ENZYMES IN THE BODY AND INTERFERE WITH PROMOTES TISSUE HYPOXIA NORMAL REACTIONS THAT OCCUR CO’S AFFINITY DAMAGES HEME ENZYMES => ANEMIA BLOCKS THE RELEASE OF GLUTAMATE => EXPOSURE DURING NEUROLOGIC DEVELOPMENT CAN RESULT IN LEARNING DISORDERS, HYPERACTIVITY, AND ATTENTION PROBLEMS CELLULAR INJURY (CONT’D) ASPHYXIAL INJURIES CAUSE: FAILURE OF CELLS TO RECEIVE OR USE OXYGEN INFECTIOUS INJURIES INVASION AND DESTRUCTION TOXIN PRODUCTION PRODUCTION OF HYPERSENSITIVITY REACTIONS CELLULAR INJURY (CONT’D) IMMUNOLOGIC AND INFLAMMATORY INJURIOUS GENETICS AND INJURIES EPIGENETIC FACTORS PHAGOCYTIC CELLS & IMMUNE AND NUCLEAR ALTERATIONS: ALTERATIONS INFLAMMATORY SUBSTANCES (HISTAMINE, IN THE PLASMA MEMBRANE STRUCTURE, ANTIBODIES, LYMPHOKINES, COMPLEMENT SHAPE, RECEPTORS, OR TRANSPORT CASCADE, PROTEASES) MECHANISM CAUSE MEMBRANE ALTERATIONS SICKLE CELL ANEMIA OCCUR AFTER CELLULAR INJURY OR INFECTION ARE CAPABLE OF DAMAGING NORMAL (UNINJURED AND UNINFECTED) CELLS CELLULAR INJURY (CONT’D) INJURIOUS NUTRITIONAL IMBALANCES ESSENTIAL NUTRIENTS ARE REQUIRED FOR CELLS TO FUNCTION NORMALLY PROTEINS, CARBOHYDRATES, LIPIDS, AND VITAMINS ALTER CELLULAR STRUCTURE AND FUNCTION, ESPECIALLY TRANSPORT MECHANISMS, CHROMOSOMES, NUCLEUS, AND DNA CELLULAR INJURY (CONT’D) TEMPERATURE EXTREMES AND CLIMATE CHANGE HYPOTHERMIC INJURY SLOWS CELLULAR METABOLIC PROCESSES (SLOWS NA-K+-ATPASE PUMP) PRODUCES REACTIVE OXYGEN SPECIES HYPERTHERMIC INJURY MAY AFFECT PULMONARY RESPONSES TO HYPOXIA OR INCREASED CARBON DIOXIDE OVERHEATING; SUDDEN INFANT DEATH SYNDROME CELLULAR INJURY (CONT’D) IONIZING RADIATION ANY FORM OF RADIATION CAPABLE OF REMOVING ORBITAL ELECTRONS FROM ATOMS X-RAYS, GAMMA RAYS, ALPHA AND BETA PARTICLES MECHANISM OF DAMAGE DETERMINISTIC EFFECTS: OCCUR ABOVE A THRESHOLD DOSE AND HAVE DOSE-RELATED INCREASED RISK DERMATITIS, ERYTHEMA, CATARACTS STOCHASTIC EFFECTS: CELL GENERATION OR HEREDITARY EFFECTS AND CANCER (UNRELATED TO THRESHOLD). OUTCOME RELATED TO TISSUE AND STRESS RESPONSE INSTEAD OF DOSE EFFECTS OF IONIZING RADIATION SOMATIC: DERMATITIS, ERYTHEMA, ETC GENETIC MUTATIONS (DNA DAMAGE) AND CHANGES IN GENETIC EXPRESSION (NOT SEQUENCING) FETAL CELLULAR INJURY (CONT’D) IONIZING RADIATION (CONT’D) BYSTANDER EFFECTS: CELLS NOT IN THE DIRECTLY RADIATED FIELD ARE AFFECTED BY THE RADIATION; REFERRED TO AS HORIZONTAL TRANSMISSION. GENOMIC INSTABILITY: GENERATIONS OF CELLS DERIVED FROM AN IRRADIATED PROGENITOR CELL APPEAR NORMAL, BUT TIME LETHAL (I.E., IRREVERSIBLE) AND NONLETHAL MUTATIONS APPEAR; REFERRED TO AS VERTICAL TRANSMISSION.  MANIFESTATIONS OF CELLULAR INJURY CELLULAR ACCUMULATIONS (INFILTRATIONS) INFILTRATIONS OCCUR IN RESPONSE TO SUBLETHAL INJURY AND IN NORMAL (BUT INEFFICIENT CELLS) EXCESSIVE AMOUNTS OF NORMAL CELLULAR SUBSTANCES SUCH AS WATER, PROTEINS, LIPIDS, AND CARBS PRESENCE OF ABNORMAL CELLULAR SUBSTANCES ENDOGENOUS: BYPRODUCTS OF ABNORMAL METABOLISM EXOGENOUS: INFECTIOUS AGENTS OR MINERALS HARM CELLS BY “CROWDING” ORGANELLES AND BY CAUSING EXCESSIVE (AND SOMETIMES HARMFUL) METABOLITES MANIFESTATIONS OF CELLULAR INJURY (CONT’D)  CELLULAR INFILTRATIONS PROTEINS WATER EXCESS ACCUMULATES PRIMARILY IN THE RENAL CELLULAR SWELLING CONVOLUTED TUBULE AND IN THE IMMUNE B LYMPHOCYTES LIPIDS AND CARBOHYDRATES PIGMENTS USUALLY AFFECTS THE LIVER (E.G., FATTY LIVER) MELANIN, HEMOPROTEINS, BILIRUBIN CALCIUM GLYCOGEN DYSTROPHIC CALCIFICATION, PSAMMOMA OBSERVED IN GENETIC DISORDERS: BODIES, METASTATIC CALCIFICATION GLYCOGEN STORAGE DISEASES URATE: URIC ACID ACCUMULATION: EXCESSIVE VACUOLATION OF THE CYTOPLASM EXCESS CAUSES GOUT MANIFESTATIONS OF CELLULAR INJURY (CONT’D) SYSTEMIC MANIFESTATIONS FATIGUE AND MALAISE LOSS OF WELL-BEING ALTERED APPETITE FEVER LEUKOCYTOSIS INCREASED HEART RATE PAIN OTHER SIGNS AND SYMPTOMS CELLULAR DEATH TWO TYPES OF CELLULAR DEATH: 1. NECROSIS INCLUDES INFLAMMATORY CHANGES 2. APOPTOSIS NO INFLAMMATORY CHANGES TYPE 1—CELL DEATH (CASPASES) TYPE 2—AUTOPHAGIC CELL DEATH CELLULAR DEATH: NECROSIS NECROSIS SUM OF CELLULAR CHANGES AFTER LOCAL CELL DEATH AND THE PROCESS OF CELLULAR AUTODIGESTION (AUTOLYSIS) NECROSIS PROCESSES 1. CELL DEATH ANDPROGRESSION TO NECROSIS (CLUMPING OF GENETIC MATERIAL, INTERRUPTION OF PLASMA AND ORGANELLE MEMBRANES) 2. KARYOLYSIS NUCLEAR DISSOLUTION AND CHROMATIN LYSIS 3. PYKNOSIS SHRINING AND CLUMPING OF THE NUCLEUS 4. KARYORRHEXIS FRAGMENTATION OF THE NUCLEUS AND DISSOLUTION  CELLULAR DEATH: TYPES OF NECROSIS COAGULATIVE NECROSIS HYPOXIA LEADS TO PROTEIN DENATURATION= CHANGES IN ALBUMIN = COAGULATION ABNORMALITY IN INTRACELLULAR CALCIUM KIDNEYS, HEART, AND ADRENAL GLANDS LIQUEFACTIVE NECROSIS ISCHEMIA = DEATH OF NEURONS AND GLIAL CELLS IN THE BRAIN HYDROLYTIC ENZYMES FORM LIQUID-FILLED CYST OR FORMS PUS  CELLULAR DEATH:TYPES OF NECROSIS (CONT’D) CASEOUS NECROSIS COMBINATION OF COAGULATIVE AND LIQUEFACTIVE NECROSES USUALLY CAUSED BY TUBERCULOSIS PULMONARY INFECTION CHEESE-LOOKING SUBSTANCE THAT IS WALLED OFF FAT NECROSIS ACTION OF LIPASES BREAST, PANCREAS, OTHER ABDOMINAL ORGANS CELLULAR DEATH: TYPES OF NECROSIS (CONT’D) GANGRENOUS NECROSIS = A CLINICAL TERM DESCRIBING DEATH OF TISSUE HYPOXIA FOLLOWED BY BACTERIAL INFECTION = CELL DEATH AND NECROSIS DRY GANGRENE = RESULT OF COAGULATIVE NECROSIS WET GANGRENE = RESULT OF NEUTROPHIL INVASION CAUSING LIQUEFACTIVE NECROSIS GAS GANGRENE = INFECTION OF INJURED TISSUE BY CLOSTRIDIUM SPP. CELLULAR DEATH: APOPTOSIS APOPTOSIS IS PROGRAMMED CELLULAR DEATH THAT OCCURS IN NORMAL AND PATHOLOGIC CELLS CHARACTERIZED BY THE “DROPPING OFF” OF CELLULAR FRAGMENTS CALLED APOPTOTIC BODIES DYSREGULATED APOPTOSIS: EXCESSIVE RATE OF APOPTOSIS = NEURODEGENERATIVE DISEASES AND ISCHEMIC INJURY INSUFFICIENT RATE OF APOPTOSIS = CANCER AND AUTOIMMUNE DISORDERS CELLULAR DEATH: AUTOPHAGY SELF-DESTRUCTIVE “RECYCLING” PROCESS SURVIVAL MECHANISM: CANNIBALIZES CELLS WITH BAD ORGANELLES OR ABNORMAL PROTEINS AND REUSES THE GOOD STUFF EX) METABOLIC STRESS CONDITIONS: AUTOPHAGY ALLOWS ATP AND OTHER ENERGY SOURCES (MITOCHONDRIA AND ER) TO BE REUSED AFTER THE ORIGINAL CELL HAS UNDERGONE EXCESSIVE STRESS QUESTIONS? 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