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Pathophysiology Weeks 1-2 Notes Revised

by: Haley

Pathophysiology Weeks 1-2 Notes Revised NURS 239 001

Marketplace > University of New Mexico > Nursing and Health Sciences > NURS 239 001 > Pathophysiology Weeks 1 2 Notes Revised
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About this Document

These notes cover cell structure, immunity, and adaptation. They are revised from the previous set I posted, so get these instead!
Pathophysiology I
Class Notes
pathophysiology, patho, Nursing, cells, Immunity
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This 9 page Class Notes was uploaded by Haley on Saturday January 30, 2016. The Class Notes belongs to NURS 239 001 at University of New Mexico taught by Drexler in Fall 2015. Since its upload, it has received 26 views. For similar materials see Pathophysiology I in Nursing and Health Sciences at University of New Mexico.

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Date Created: 01/30/16
• Patho Exam 1 Notes (part 1) • Chapter 1 • Cell Components and Functions ◦ Cytoplasm ◦ Organelles ▪ Endoplasmic Reticulum: smooth and rough variety; synthesizes proteins (protein metabolism) ▪ Golgi apparatus: packages proteins and sorts them ▪ Lysosome: gets rid of waste ▪ Peroxisome: like peroxide; bubbles and then neutralizes free radicals ▪ Proteasome: breaks down proteins ▪ Mitochondria: produce ATP (ENERGY!!) ◦ Nucleus: stores DNA ◦ Cytoskeleton: made of tubules, filaments; ▪ Allows for movement and transfer; ▪ Its shape = its function in the body • Functions of Cells ◦ Movement: cells are mobile and travel ▪ Cytoskeleton ◦ Conductivity: cells have electric potential ▪ Heart ▪ Brain ◦ Metabolism: cells use nutrients for activity ◦ Secretion: cells synthesize substances ▪ Hormones ◦ Excretion: get rid of waste ◦ Respiration: exchange of O2 to CO2 ▪ This is DIFFERENT from ventilation: the act of taking in air and exhaling ◦ Reproduction: cells make new tissue ◦ Communication: cells direct signals throughout the body ▪ Hormones ▪ Neurotransmitters • Passive Movement ◦ Diffusion: movement of particles ▪ Particles are doing the moving ◦ Osmosis: movement of water to disperse particles ▪ Water is doing the moving • Active Transport ◦ Uses channels and energy (ATP) ▪ Sodium-potassium pump • Facilitated Diffusion ◦ Channel is opening bigger to compensate for large particle ◦ The channel pulls the large particle inside • Types of Ingestion ◦ Endocytosis: type of active transport where cell engulfs the particle ◦ Pinocytosis: cellular drinking ◦ Phagocytosis: cellular eating ◦ Exocytosis: transport out of cell with particle packaged into a vesicle • Respiration ◦ Anaerobic ▪ Fermentation occurs in cytosol ▪ NO OXYGEN ▪ 2 ATP ◦ Aerobic ▪ Uses oxygen to produce energy ▪ Occurs in mitochondrion ▪ 32 ATP • Communication ◦ Receptor-ligand binding: on and off mechanism of communication ◦ Feedback mechanisms: a loop system to maintain homeostasis ▪ Positive: enhances effects of stimulus ▪ Negative: loop that increases and then decreases effects of stimulus =0 • Reproduction ◦ Proliferation: cells are actively dividing ▪ Mitosis ▪ Meiosis ◦ Differentiation: cells have already divided and are changing into a specific functional cell • Chapter 3 • Atrophy: cells shrink ◦ Neural atrophy: brain cells shrink ▪ Brain is not “exercise” and connections fade, causing cells to shrink ▪ Older people need stimulation: Sudoku, crosswords ◦ Muscular atrophy: muscle cells shrink ▪ A broken arm is atrophied from no use while in cast • Hypertrophy: cells increase in size ◦ Overuse ▪ Muscles increase size when weight training because stress signals are sent to the cells to increase size to accommodate for the increased load of the weights • Hyperplasia: an increase in the number of cells ◦ Damage; occurs in inhospitable environments ◦ Smoking: cells in lungs change type black lung • Metaplasia: change in the structure and number of cells ▪ Menstruation: Female hormones cause the uterus to shed it’s lining when the cells have been damaged from ovulation, intercourse, etc. ▪ GERD: acid reflux destroys cells in digestive system • Calcium based products reduce acid • Dysplasia: disorganized change in number, size and structure of cells ◦ Cancer: cells proliferate rapidly in a disorganized fashion ◦ Autocrine hormones • Cell Injury ◦ Stress is induced ▪ Increased demand placed on cellsadaptation • Hypertrophy  • Hyperplasia • Atrophy • Metaplasia • Dysplasia  • Storage ◦ Normal cell ▪ Reversible cell injury (mild)normal cell ▪ Reversible cell injury (severe)cell death • Causes of Cell Injury and Death ◦ Hypoxia: cells have no oxygen ◦ Oxidative stress: continuous “poking” (damage points) of cell to cause breakage and stress ▪ Free radicals are unbound oxygen particles that hit (poke) the cell and cause pain (damage) ◦ Accumulations: pimples, sunburns, blisters ▪ Fluid build up ◦ Mechanical: stabs, gunshots, direct impact ◦ Thermal: frostbite, fever ▪ Freezing cells: hypothermia: preserves cell function by slowing down cellular processes ▪ Fever: vasodilationreleases heat ◦ Apoptosis: programmed cellular death • Cerebral Atrophy ◦ Neuron cells in cerebrum shrink ◦ Why: ▪ Not enough stimulation ▪ Injury ▪ Hypoxia ◦ Focal: localized section of the brain ◦ Global: affects whole brain ▪ Frontal lobe: judgment, memory, personality ▪ Hippocampus and cortex: memory, comprehension ▪ Basal ganglia: movement ◦ Diagnostic ▪ Find loss of function early ▪ Neuro exam ▪ Physical ▪ Brain Imaging ◦ Treatment ▪ Prevention ▪ Interrupt process of injury • Keep mind active ▪ Slow disease • Cardiac Hypertrophy: increase in cardiac muscle mass ◦ Caused by: ▪ Excessive cardiac workload ▪ Increased functional demand ▪ Genetics ◦ Primary: genetic non-sex linked trait ◦ Secondary: condition increases the left ventricle’s workload increase in myocardial cell size ◦ Symptoms ▪ Shortness of breath ▪ Syncope: pass out due to low O2 ▪ Impaired cardiac function ◦ Diagnostic ▪ Genetic tests ▪ Hypertension ▪ Low exercise tolerance ▪ Arrhythmia (irregular beat) ▪ Altered cell signals ▪ Heart murmur ◦ Treatment ▪ Surgical: new heart or device ▪ Medication • Ventricle relaxation • Workload reducers ▪ Decrease pressure ▪ Physical Activity restriction • Acromegaly ◦ Caused by: ▪ Hyperplasia ▪ Excessive pituitary growth hormone and liver insulin-like growth factor stimulation ◦ Excessive growth of bones, cartilage, soft tissues, organs ◦ Hormones release after epiphyseal plate closes ◦ Appearance ▪ Soft tissue swelling ▪ Altered face features ▪ Pain/numbness in hands ▪ Skin changes: darkening ◦ Other symptoms ▪ Snoring ▪ Voice deepening ▪ Sterility ▪ Hyperplasia of heart ◦ Diagnostic ▪ Medical history ▪ Physical ▪ Lab test ▪ Glucose tolerance test ▪ Excess growth hormone ◦ Treatment ▪ Supportive care ▪ Medicine • Cervical Metaplasia and Dysplasia ◦ Epithelial cells of the transformation zone in the cervix adapt in one of two ways ▪ Metaplasia ▪ Dysplasia ◦ Manifestations ▪ No signs or symptoms ▪ Early sex: longer time frame for something to be acquired ▪ More than 3 partners ▪ Smoking ▪ HPV ◦ Diagnostic ▪ Medical History ▪ Physical ▪ Screening tests ▪ Micro exam of the transformation zone ▪ HPV screening ▪ Biopsy of cervical tissues • Cone biopsy: go into layers of cells to see how far the cells have changed ◦ Treatment ▪ Reduce sexual activity ▪ Eliminate damaged cells ▪ Freeze cells ▪ Surgery • Environmental Toxins and Cardiovascular Disease ◦ Environmental chemicals cardiovascular cell injury ◦ Free radicals cause cell damage ◦ Normal Mild atherosclerosis (hardening of fats)severe atherosclerosis ◦ Manifestations ▪ Aortic aneurysm ▪ Chronic lung disease ▪ Cancer ▪ Pneumonia ▪ Chronic lung disease ▪ Coronary ▪ Stroke ◦ Thrombus: blockage in artery ▪ Blockage in carotid artery ▪ Blockage in cerebral artery ◦ Cardiovascular and Respiratory Complications ▪ Low exercise tolerance ▪ Difficulty breathing ▪ Blood clot ▪ Hypertension ▪ Increased heart rate ▪ Lower cardiac output ▪ High LDL levels ▪ Sclerosis ◦ Diagnostic ▪ Medical history ▪ Physical ▪ Lab tests ◦ Treatment: ▪ Reduce risks: less smoking or change environments ▪ Manage symptoms ▪ Drugs that lower blood pressure ▪ Drugs assisting with smoking management • Chapter 5 • Lines of Defense ◦ Skin and mucous membranes ◦ Inflammation: triggered by tissue injury ◦ Immune Response ▪ Edema: leakage of plasma proteins • Goals of Inflammation ◦ Get more blood flow to site of injury ◦ Bring more healing cells to site ◦ Get tissue ready for repair ▪ Mast cell releases IGEinflammationallergies ▪ Itis= inflammation • Vascular Response: blood and veins ◦ Chemical mediators help vascular response be faster ◦ Vasodilation makes capillaries more permeable ◦ Goal: increase blood flow at injured area • Inflammatory Mediators: cells that help inflammation process ◦ Cell variety mediators ▪ WBCs (white blood cells) ▪ Platelets ▪ Endothelial or damaged tissue ◦ Plasma variety mediators ▪ Complement system: helps vasodilation • Complement proteins: create hole (pore) in plasma membrane for inrushing fluids ▪ Kinin system: helps vasodilation • Bradykinin: stimulates nerve endings and vasodilates ▪ Clotting system • Intrinsic Pathway of coagulation • Extrinsic Pathway of coagulation ◦ Antibodies: ▪ Antibodies attach to antigens to prevent the pathogen from entering the cell ▪ Antibodies make pathogens clump together: larger size= less room for pathogen to get in ▪ Antibodies activate complement proteins ▪ Complement proteins cause pathogen to burst • Order of Events in Inflammation ◦ Erythma: redness, warmth due to increased blood flow ◦ Edema: increased vascular permeability and leakage of fluid ◦ Cellular inflammation: pus ◦ Thrombosis: formation of blood clots ◦ Stimulation of nerve endings: pain ▪ Vasocontriction= decreased blood flow and decreased stimulation of nerve endings • Cellular components of inflammation ◦ Key cell players: B cells, T cells, Natural Killer cells (lymphocytes) ▪ 70% neutrophils ▪ 30% Natural killer cells ◦ Receptors: receive signals and incoming cells ◦ Products: Cytokines, chemokines, interleukins, interferon ◦ Mast Cells ▪ Release histamine, constrict smooth muscle, dilate venules ▪ Degranulation: releases antimicrobial cytotoxic particles to impare pathogens ◦ Basophils ▪ Leukotrienes: have smooth muscle constriction (slower than mast cells) • Increase vascular permeability ▪ Prostaglandins: more vascular permeability • Clean up neutrophils (chemotaxis: responding to chemical signals and moving) • Cause pain • Cellular Response ◦ Chemotaxis: clean up of cell (help call) ◦ Cellular adherance: cells attach to the endothelial lining of another cell ◦ Cellular migration: cells slip through a gap to help ◦ Diapedesis: cellular walking ▪ cells use diapedesis to migrate


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