Cell Biology Review and Altered Functions. Embryonic Stem Cells.
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Transcript of Cell Biology Review and Altered Functions. Embryonic Stem Cells.
Cell Biology
Review and Altered Functions
Embryonic Stem Cells
Man Made Stem Cells
Adult Stem Cells
Major Parts
Eukaryotic Cell Structure
Cell Functions
CommunicateAbsorbSecreteExcreteRespireMoveConductReproduce
What is the “Brain” of the cell?
Cell Membrane (“membrain”)
StructureFunctionReceptorsJunctionsSignal TransductionTransport Gradients
ConcentrationDependentIndependent
Electrical Pressure
Bulk Transport
Cell Membrane Proteins
Na+/K+ Pump
Cell Junctions
Adhesion Molecules
Cell Adhesion Molecules (CAM)Bind growth factors
CadherinsBind cell membranes to form junctions
SelectinsBind WBCs during inflammatory reactions
IntegrinsBinds extra cellular matrix proteins
Cell Junctions
Cancer Metastasis
Cell Signals
Hormone vs. Neurotransmitter
Target Cell
Receptors
Cell Receptor Summary
Abnormal Intercellular Communication
Alterations in Membrane:
enzymes, ionsreactive oxygen species
(ROS) Adhesion molecules:
defense, clotting, metastasis
Gradients: water, ions, glucose
Transport Proteins: pumps, channels
Signaling molecules: hyper/hypo production
Receptors: destroyed, blocked,
triggered
Mitochondria
Cellular Metabolism
MacromoleculesEnergy Requirements:
BMR, TMR
Energy FormsMetabolic Pathways
Glycolysis Aerobic Respiration Beta Oxidation Deamination
Metabolic Pathways: Aerobic
Krebs Cycle
Metabolic Pathways: Proteins & Lipids
Metabolism Summary
Metabolic Alterations Alterations
Impaired Input MalnutritionMalabsorption
Impaired BalanceHypoxiaToxicityTraumaGenetic
Demand ChangesHypometabolic State
• Aging,• Immobility
Hypermetabolic State• Pregnancy• Hypothermia• Wound healing• Stress
Alcohol Metabolism
Cell Cycle
Cell Divisions Compared
Tissue Types
Tissues
RepairRegenerationScar Tissue
DeathApoptosisNecrosis
Mechanisms of Cellular Injury
Response depends on Type of injury Duration Severity
Consequences depend on Type of cell Current physiology of cell Adaptability
Vulnerable cell sites Cell Membrane Mitochondria Nucleus
Hypoxia Ischemia Oxidants
Causes of Cellular Injury
PhysicalChemicalMicrobialImmunologicGeneticNutritionalAging
Toxic, Chemical, or Physical Injury
ChemicalEnvironmental agentsDrugsMetabolites
PhysicalTraumaTemperatureRadiation
Heat Injury to RBCs
Pathogenesis example
Sequella to injury
Changes due to injury
Reversible Injury Processes
Transient if stress is removed Compensatory responses
Full capacity to repair Adaptation with diminished
capacity Cell Responses
Cell swelling (hypertrophy)Na+/K+ pump damagedOsmosis
Fatty changesCell metabolism changesSevere injurySlower to recover
Reversible Injury in the LiverGross Findings
GreasyPaleEnlarged
Cellular Metabolism StopsDisruption of Beta
OxidationFA TriglyceridesCytoplasmic fat
droplets
Fatty Liver
Hypoxia and Ischemia
Define HypoxiaEnd results
ATP production changes
Anaerobic mechanismspH changes
Organ DiseasesLungsHeartBlood VesselsBlood
Define IschemiaEnd results
Hypoxia Infarct
Organ problemsArteriesVeins
Ischemia Infarct Necrosis
Coagulative necrosis in the kidney
Ischemia Pathway
Reversible Injury from Hypoxia/Ischemia
Decreased Oxidative phosphorylation
Decreased ATPDepletion of glycogenDecreased pHDecreased protein
synthesisElectrolyte changes
Na+ K+ Ca++
Increased osmosisSwollen organelles
Small Intestine
Stress and Intracellular Changes
CytoskeletonLysosomesMitochondriaSERIntracellular
accumulationsFatProteinGlycogenPigmentsCholesterol
Stressors and Cell Death
Lipofuscin Pigment in hepatocytes
Irreversible Injury from Hypoxia/Ischemia
Cell Membrane injury Free radical formationLipid breakdownLysosomal enzyme
release Ribosomes Nuclear changes Protein digestion
Ca++ accumulates in mitochondria
Activation of Inflammatory chemicals
Lung
Pathological Calcification
Dystrophic CalcificationOccurs in dead, dying, or damaged tissue
AtherosclerosisHeart Valves
Metastatic CalcificationOccurs in hypercalcemic states
Renal FailureSecondary Hyperparathyroidism
Free Radical Formation and Damage
Effects of Oxidative Stress
Enzymes involved in Oxidative Stress
Mitochondrial Function and Damage
Mitochondrial Damage
Release of Cytochrome C
Mitochondrial Changes in Injury
DNA damage
Antioxidants
Reversible vs Irreversible DamageCardiac Function
Cellular Adaptations
PhysiologicUp or down regulationProtein synthesisAtrophyHypertrophyHyperplasia
Pathological AtrophyHypertrophyHyperplasia /
DysplasiaMetaplasia
Atrophy
Hypertrophy
Hypertrophic Cardiomyopathy
Hyperplasia
Metaplasia and Dysplasia
Necrosis Morphological Types
Coagulative Necrosis Protein coagulation due to acidosis MI
Liquefactive Necrosis Complete digestion of dead cells Nervous system, Bacterial and Fungal Diseases
Gangrenous Necrosis Ischemic coagulative necrosis Post op
Caseous Necrosis Amorphous granular debris (cheese like appearance) TB infections
Fat Necrosis Fat destruction due to liquefaction Fatty acids combine with calcium to create chalky white areas (saponification) Pancreatitis
Liquefactive Necrosis in the brain
Necrosis
Caseous Necrosis (lung)
Gangrenous Necrosis
Skin
Apoptosis
Differences between cell death:Necrosis and Apoptosis
Necrosis Contiguous cells Membrane loss Gradient changes Organelles swell Nucleus
Pyknosis (shrinks)Karyorrhexis (fragment)
Apoptosis Individual cells Normal process Cells shrink Fragmented bodies Phagocytosis
Factors in Cell Death
Necrosis stimulates inflammation
Tissue Repair
Tissue TypesParenchymal (fxn)Stromal (CT)
RepairRegenerateReplacement
Regenerating AbilityLabile cells Stable cells Permanent cells
Tissue Repair and Chronic injury
Cellular Aging Theories
Cellular SenescenceLoss of redundant DNA sequencesRadom errors/mutations/repair Free Radical DamageTelomere ShorteningDecreased heat shock responseGlycosylation of proteins and NAMetabolic Rate (inverse)Homeostatic Systems decline
Cellular Damage vs Repair Cycle
Summary of Cellular Damage Events
Examples of someDiseases/ConditionsCaused by alterations In Cell Function
Questions?