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Understanding Pathophysiology

by: Jazmine Morales

Understanding Pathophysiology Nurs 20363

Marketplace > Texas Christian University > Nurs 20363 > Understanding Pathophysiology
Jazmine Morales
GPA 3.7

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These objectives cover chapters 2 through 12
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This 21 page Study Guide was uploaded by Jazmine Morales on Saturday September 10, 2016. The Study Guide belongs to Nurs 20363 at Texas Christian University taught by Cheek in Fall 2016. Since its upload, it has received 7 views.


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Date Created: 09/10/16
 Discuss common chromosomal mutations. Trisomy 21= Down syndrome  most common among live born infants 1 in 800 births  many individuals share skin, hair, and eye color  have many features but not every person has them all  affect males and females and all races equally  thicker lips w/ slightly protruding tongue  congenital heart defects  flat faces  slightly low­set ears  wide gap between 1  and 2  toes  widely spread eyes  palmar on simian crease across palms  decreased intellectual development  poor muscle tone and reflexes at birth  premature aging  increased risk for leukemia  leukemia markers on chromosome 21 and they  have 3 copies of the chromosome Trisomy 18= Edward syndrome 1 in 3000 to 5000 births  Affects females more often than males  Most are stillborn, or usually die within a year  Features: clenched hands w/ overlapping fingers, shield chest or short sternum,  small mouth/jaw and short neck, wide­set nipples, flexed big toe, prominent heels Trisomy 13  Cleft lip or palate  Malformed ears  Clenched fists or polydactyly/ extra fingers  Undescended or abnormal testes  Absent eyebrows Extra X chromosome= common occurrence  Occurs in males and females  Single extra X associated w/ few phenotypic manifestations  Multiple extra X’s more problematic Trisomy X= karyotype shows 47, XXX 1 in 300 to 400 births  All races equally affected  Normal female phenotype  Height greater than average and greater than siblings  Slight delay in language and motor skills  Fertility unaffected Klinefelter syndrome= karyotype shows 47, XXY1 in 600 births  Normal infant and childhood male phenotype  Some association w/ advanced paternal age  Number is undefined  All races equally affected  Features in adults: taller than average, low testerone levels, high FSH levels,  loss of secondary sexual characteristics, higher incidence of ADHD and autism,  small testes and  penis, gynecomastia, decreased libido, diabetes, thyroid  disease, SLE, Azoospermia  Infertility is high for men Monosomy X= Turner syndrome most common chromosome problem conceived 45, X  Most conceptions lost as 99% miscarriages  1 in 1500 to 2500 female births  Intellectual functioning patterns same as general population  Features: web­neck appearance, shorter stature, discolored spots on skin, extra  skin, mainly females, swollen hands, decreased growth rate  No adolescent growth spurt  Broad, shield­like chest  Kyphosis, scoliosis  Osteoporosis   Articulate common genetic mutations such as missense, nonsense, and  frameshift Silent point mutation= single base change in the DNA only but no change in AA sequence                     **does not change protein function Missense= single base change that causes a different AA to be placed within the protein                     **reduces protein function, causes change Nonsense=single base change that results in a “STOP signal” that halts protein synthesis                     **Eliminates protein function** Produces 1 of the 3 stop codons in the mRNA                      terminates translation Frameshift= point mutation with an insertion or deletion of a number of bases not divisible by 3                       **Change the entire reading frame of DNA sequence bc the deletion or insertion is                       not a multiple of 3 base pairs in a codon Describe cellular level genetics: DNA, RNA, proteins, etc.(self study)  Genes= basic units of inheritance are composed of DNA located on the  chromosomes  DNA= composed of deoxyribose, a phosphate molecule, and 4 nitrogenous  bases; physical structure= double helix  AG= purines; TC= pyrimidines A pairs with T; C pairs with G  Bases= nucleoproteins  DNA bases code for amino acids, which make up proteins  DNA replication is based on complementary base pairing, in which a single  strand of DNA serves as the template for attracting bases that form a new strand  of DNA  double strand  DNA polymerase= enzyme involved in replication adds bases to the new DNA  strand and performs “proofreading” functions  Mutation= inherited alteration of genetic material  Transcription & translation= 2 basic processes in which proteins are specified  by DNA, both involve RNA  RNA= similar to DNA, but is single stranded, has a ribose sugar molecule, and  has uracil rather thymine similar to thymine so uracil can also pair with adenine  Proteins= composed of one or more polypeptide, which in turn consists of  sequences of amino acids; body has 20 different AA w/ only 4 base, different  combinations of bases, occurring in groups of 3, these triplets are codons  Codons= specifies a single AA in a corresponding protein  All living organisms use the same DNA codes to specify proteins except for mitochondria 5.  Recognize and use standard pedigree symbols.  Study page 50 6.  Understand the importance of genetics in modern healthcare. Better understanding of genetics promises a future of precise, customized medical treatments  Whole genome sequencing provides a nearly complete DNA sequence of an individual’s genome allows researchers to identify genes suspected of causing a disease/disorder and estimate an individual’s risk of a future medical condition Knowing the DNA sequence of a gene reveals the basic structure of the protein the genes encodes  Researchers are using genetic engineering to diagnose and predict disease, and to develop therapies and drugs to treat devastating diseases like cancer, Alzheimer's, diabetes, and cystic fibrosis.  Other reasons for sequencing patients’ genomes are to tailor cancer treatments and better understand how certain drugs can affect patients  Once Scientists figure out what DNA sequence changes in a gene can cause disease, healthy people can be tested to see whether they risk developing conditions like heart disease, diabetes, or prostate cancer Pharmacogenomics tailoring drugs for patients, whose individual response can be predicted by genetic fingerprinting; what would be the safest and most effective dose?  Newborn screening  Carrier screening  Gene therapy  Gene-based therapy  Recombinant DNA can be used to develop drugs, vaccines, and to reproduce important human hormones and proteinsEX: insulin production 7.  Know the difference between single gene disorders, multifactorial conditions.  Single gene disorders include: Achondroplasia, CF, Hemophilia, Marfan syndrome, Huntington disease, Hurler syndrome, Sickle cell trait, Syndactyly, Sickle cell disease, Muscular dystrophy, and PKU Multifactorial inheritance= environmental factors that influence the expression of a trait EX: IQ and height  Recurrence risks for multifactorial diseases becomes higher if more than one biologic family member is affected or if the expression of the disease is the proband  A certain threshold of liability must be crossed before the disease is expressed.  Below the threshold the individual appears normal, above it, the individual is affected by the disease Below= normal, Above= affected  Multifactorial conditions include: Pyloric stenosis narrowing or obstructing of the pylorus sphincter (between stomach & SI), chronic vomiting, weight loss, constipation, electrolyte imbalance, cleft lip, cleft palate, neural tube defects, clubfoot Objectives for Chapter 4: 1. Describe atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia. Atrophy= decrease or shrinkage in cellular size;   can affect any organ, but is most common in skeletal muscle, the heart,  secondary sex organs, and brain  Classified as physiologic (early development) or pathologic(decreases in  workload, pressure, use, blood supply, nutrition, hormonal stimulation) Hypertrophy= increase in the size of cells in response to mechanical stimuli; increases size of affected organ Examples of mechanical load/ stress  Repetitive stretching  Chronic pressure  Volume overload Hyperplasia= increase in the number of cells, resulting from an increased rate of cellular division In response to injury, when the injury has been severe and prolonged enough to have caused cell death  Compensatory hyperplasia= adaptive mechanism that enables certain organs to regenerate  Hormonal hyperplasia= occurs in estrogen-dependent organs, such as the uterus & breast Dysplasia= abnormal changes in the size, shape, and organization of mature cells not a true adaptive change, does not indicate cancer  Often called atypical hyperplasia Metaplasia= reversible replacement of one mature cell type by another. It is thought to develop, as an adaptive response better suited to withstand the adverse environment, from a reprogramming of stem cells 2.  Identify the mechanism of cellular injury from hypoxia­­specifically ischemia  and anoxia. Mechanisms of cellular injury from hypoxia:  Activation of immune responses & oxygen­sensing compounds called prolyl  hydroxylases (PHDs) & hypoxia­inducible transcription factor (HIF) HIF= family of transcription regulators that coordinate the expression of many genes in  response to oxygen deprivation  Ischemia= most common cause of hypoxia (reduced blood supply)  Caused by gradual narrowing of arteries (arteriosclerosis) or complete blockage  by blood clots (thrombosis)  Anoxia= total loss of oxygen caused by sudden obstruction such as an embolus Mechanisms for ischemia reperfusion injury:  Oxidative stress= injury induced by free radicals, especially by reactive oxygen  species  Occurs when excess ROS overwhelm endogenous antioxidant systems 3.  Describe the effects of street drugs and alcohol abuse to the cell and subsequently organs of  the body. Marijuana:  3­4 joints/day= 20 cigarettes/day (1 pack)  5­10% is absorbed through lungs  Increases heart rate, blood pressure  Reduced fertility, decreased sperm motility & decreased levels of circulatory testerone  Fetal abnormalities include low birth weight  Increased frequency of infectious illness Methamphetamine:  CNS stimulant   Increased metabolism  Feelings of euphoria  Aggressive (violent) behavior, anxiety, excitement, paranoia  (delusions/psychosis)  Mood changes from friendly to hostile   Increased energy, perception & alertness Cocaine/crack:  Potent CNS stimulant   Can lead to hypertension. Tachycardia, severe vasoconstriction   Blocks reuptake of neurotransmitters  Stimulus can affect narrowing of arteries; ischemia  Effects on fetus= stillbirth, retarded fetal development, premature labor,  hyperirritability Heroin:   Highly addictive; withdrawal causes intense fear  Acts on receptors such as endorphins   Infectious complications esp. Staph aureus, granulomas of lung, septic embolism & severe pulmonary edema  Sudden death from over dosage   Decreased cardiac output  Secondary or respiratory depression Alcohol:  Leading cause of liver­related morbidity & mortality  Liver & nutritional disorders are the most serious consequences of alcoholism  Nutritional deficiencies include: magnesium, vitamin B6, thiamin & phosphorus   Folic acid deficiency    fetal alcohol syndrome   Alcohol is metabolized to acetaldehyde in the liver by 3 enzymes  Acute alcoholism= CNS stimulant  Chronic alcoholism= fatty liver, inflammation, liver disease, cirrhosis,  myocardium, hypertension, acute gastritis, regressive changes in skeletal muscle   Increases high BP, risk of alcoholism, obesity, stroke, breast cancer, suicide &  accidents Chapter 8 Describe the mechanisms of infection and cellular injury by bacteria, viruses, fungi, and parasites. Review this individually as needed­info covered by Microbiology in most cases  Bacteria cause cell injury by producing exotoxins & endotoxins Exotoxins= enzymes  that can damage the plasma membranes of host cells or can inactivate  enzymes critical to protein synthesis Endotoxins= activate the inflammatory response & produce fever (pyrogenic)  Viruses cause cell injury by using metabolic processes of host cells to proliferate & cause  disease; they disrupt lysosomal membranes, form inclusion bodies, fuse with host cells to  produce giant cells, alter antigenic properties, transform host cells into cancerous cells & promoto bacterial infection  Fungi cause cell injury by releasing toxins & enzymes that are damaging to tissues Candida  albicans most common Dermatophytes are fungi that infect hair, skin, & nails with diseases such as ringworm & athletes foot  Parasites can cause cellular injury through vector transmission of a mosquito bite or contaminated  food/water that have surface proteins allowing them to attach to receptors, infecting macrophages, RBCs, or  organ cells in the liver EX: Plasmodium occurs in erythrocytes & results in the release of additional parasites that infect other  erythrocytes Bacteriocidal= kills the microorganism Bacteriostatic= inhibits growth   Communicability= the ability to spread from one individual to others and cause disease  Immunogenicity= ability of pathogens to induce an immune response  Infectivity= the ability of the pathogen to invade and multiply in the host  Pathogenicity= ability of an agent to produce disease  Mechanism of Action=manner in which the microorganism damages tissue  Portal of Entry= route by which a pathogen infects the host  Toxigenicity= ability to produce toxins or endotoxins  Virulence= capacity of a pathogen to cause severe disease Discuss the type of Hypersensitivity reactions Type I (IgE mediated)= most common in bee stings; occur after antigen reacts with IgE on mast cells, leading to  mast cell degranulation & the release of histamine & other inflammatory responses Another words……Mast cell degranulation occurs because IgE attaches to the receptors releasing histamine  1  time= antigens are created  2  time= recognition; goes straight through process, person has worse outcome  Increases vascular permeability  Vasodilation  Contracts bronchial muscle  Edema, swelling, inflammation, hives, troubled breathing Type II (tissue­specific)= 4 possible mechanisms: complement­mediated lysis, opsonization & phagocytosis,  antibody­dependent cell­mediated cytotoxicity & modulation of cellular function Type III (immune­complex mediated)= formation of immune complexes that are deposited to target tissues, where  they activate the complement cascade, generating chemotactic fragments that attract neutrophils into the  inflammatory site can be a systemic reaction, such as serum sickness or localized antigen/antibody complexes Type IV (cell­mediated)= sensitized T cells, which either kill target cells directly or release lymphokines that activate  other cells, such as macrophages does not include antibody; no reaction Describe the stages of Selye's general adaptation syndrome (GAS) and what occurs at each stage  Dr. Selye­1946  Alarm stage  Arousal of CNS and hypothalamus (stressor activates hypothalamus & SNS)  Sympathetic nervous system, which releases norepinephrine (20%), from adrenal gland,  which causes medulla of adrenal gland to release epinephrine (80%)  Defenses are mobilized­initial fight or flight  Resistance/adaptation stage  Begins with the actions of adrenal hormones­cortisol, norepinephrine, epinephrine  Mobilization contributes to fight or flight  Exhaustion stage (allostatic overload)  Occurs only if stress continues and adaptation is not successful  Breakdown of compensatory mechanisms  Leads to stress­related disorders Describe hypersensitivity, autoimmunity, and alloimmunity Hypersensitivity= altered immunologic response to an antigen that results in disease or damage to  individual Autoimmunity= disturbance in the immunologic tolerance of self­antigens immune system reacts  against self­antigens to a degree that autoantibodies or autoreactive T cells damage tissues Alloimmunity= immunologic reaction against tissues of another individual EX: transfusions, transplants, fetus during pregnancy Define stress, identify stressors, and state the effects of stress Stress= perceived or anticipated threat that disrupts person’s well­being or homeostasis May stem from psychological/emotional (fear, social rejection), physical, physiological (inflammation,  infection) stimuli that trigger stress response Stressors: age, gender, social support, spiritual factors, coping mechanisms used/learned, genetics,  personality, self­esteem, current health, length of time of exposure to stressor, past ability/experience to  deal with stress Summarize the major interactions of the body systems involved in the stress response HPA Axis  Nervous system sympathetic branch of autonomic nervous sytem  Hypothalamus secretes corticotropin­releasing hormone (CRH)  Pituitary releases adrenocorticotropin hormone (ACTH)  Endocrine system pituitary & adrenal glands  Adrenals secrete cortisol and catecholamines(epi and nor­epi)  Immune system  Multiple alterations secondary to cortisol and catecholamines  Distinguish between effective and ineffective methods of coping with stress     Effective meth  for coping with stress support physiologic conditions that are likely to enhance protective immunity, cognitive & physical performance & overall health EX: social support, counseling   Ineffective methods  for coping with stress involves chronic or long­term biologic  changes that are likely to result in dysregulation or suppression of immune function,  decrease in cognitive & physical performance & an increase in the likelihood of disease EX: increased smoking/alcohol, change in eating habits, sleep deprivation & circadian  disruption, overcommittment to employment­related tasks, repression ,denial, escape­ avoidance & concealment are associated with immune functions Chapter 10­12 Compare cancer by cell type of origin  Cancers arising from epithelial tissues= carcinomas  Cancers arising from ductal or glandular structures= adenocarcinomas  Cancer from breast glandular tissue= mammary adenocarcinoma  Benign breast tumor= fibroadenoma  Mesenchymal tissue (CT, muscle & bone)= suffix sarcoma  Cancers of lymphatic tissues= lymphoma  Cancers of blood forming cells= leukemias Compare/contrast the characteristics of benign & malignant tumors Benign tumors:  Encapsulated do not spread; slow growing; non­invasivenon­metastatic  Well­organized stroma & well­differentiated  Generally named according to the tissues from which they arise with –oma suffix  Can become extremely large & depending on their location, can cause morbidity  or be life­threatening Malignant tumors:  No capsule locally invasive; metastatic spread to other tissue of orign  Rapid growth rates with hemorrhage & necrosis; large; poorly demarcated  Loss of differentiation (anaplasi  absence of normal tissue organization  Pleomorphic (variability of size & shape)  Dark stained nuclei; lots of stroma disorganized  Generally named according to the cell type from which they originate Explain how tumor cell markers are used Tumor markers= substances produced by both benign & malignant cells that are either present in or on tumor cells, found in blood, spinal fluid, or urine **Can also be altered for patients WITHOUT cancer** **Not enough to diagnose a specific type of cancer**  Include: hormones, enzymes, genes, antigens, & antibodies Used to: 1. Identify cancer in people with no symptoms 2. Screen individuals for cancer at an early stage 3. Diagnose specific type of tumor with clinical manifestations in individuals 4. Determine effectiveness of cancer treatment 5. Identify recurrence of cancer after treatment Explain how cancer is caused by mutations in genes and the roles of certain  genes in cellular development/cancer formation  Caretaker genes= maintains the integrity  Proto­oncogenes= genes that encode components of receptor­mediated  pathway designed to regular normal cell growth  signaling enzymes, mutated  into hyperactivity (oncogenes); cannot be inherited;   Tumor­suppressor genes= signal to stop cell growth; they get turned off  (inactivated) inhibits growth (proliferation); stop cell division when cells are  damaged & prevent mutations; mutated into inactivity to allow cancer to occur; 2  copies (one from each parent); 2 mutations are necessary germ cell mutation  results in transmission of cancer­causing genes from 1 generation to the next  Oncogenes= cancerous cells express mutated or overexpressed; oncogenes  activated in cancers; may be activated by gene amplification  List modifiable and non­modifiable factors that are related to cancer Modifiable risk factors are ones that you can change and do something about such as:  Smoking  Alcohol use  Nutritional intake/diet  Hormones  Physical activity; being overweight  High BP, high cholesterol, diabetes  Infections; sexual practices  UV exposure  Stress  Occupational carcinogens= asbestos, dyes, rubber, paint, benzol inhalation, drugs Non­modifiable risk factors are ones that you can’t do anything about such as:  Age  sex  Ethnic background  Family history  Geography  Reproductive/ menstrual traits  Genetics Discuss types of gene mutations Genetic changes may occur by both mutational & epigenetic mechanisms  Point mutations= alteration of one or a few nucleotide base pairs  Chromosome translocations= large changes in chromosome structure in which a  piece of one chromosome is translocated to another  Gene amplification= result of repeated duplication of a region of a chromosome, so that instead of 2 normal copies of a gene, 10s or even 100s of copies are present increased expression of an oncogene or drug resistance genes  Loss of heterozygosity 3 stage theory:  Initiation= produces initial cancer cells exposure  Promotion= population of cancer cells expands with diversity of cancer cell phenotypes ** Remove exposure, then cancer won’t continue to grow, but if you continue exposure,  then promotion starts  Progression= leading to a spread of tumor to adjacent & distal sites (metastasis) Role of epigenetics  Epigenetics= factors that affect how our genes are expressed; software/ expression  that gets modified  Genetics= hardware  A long latency period precedes onset of adult cancers  Cancer survival rate is (69%) for all cancer/stages  5 year survival rate  when you’re diagnosed  Number 1 cause of death in the US is heart disease, but cancer is the leading cause of  death in the world  Genetic cancer= before the age of 55  Epigenetics/pathology= 70s or 80s  DNA methylation, Histone acetylation & Non­coding RNA all sustain & initiate epigenetic  change Role of viruses in cancer  HPV  Herpes Type 2  Hepatitis B & C  Bacteria H.pylori  Epstein Barr  CMV  They compromise your immune system making you more susceptible to predisposition  of genetic mutations immunocompromised patients with HIV & SLE  Has led to the development of vaccines Analyze the association between environmental risk factors or hormones with  cancer Elevated estrogen levels Describe how tumors spread  Cancer cells are spread through vascular  & lymphatic pathways  Tumor cells bind to blood platelets, giving them a protective coat of nonmalignant blood cells that  both shields the tumor cells & creates small tumor embolus, or cancer clo,t that can promote  cancer cell survival in distant locations  The venous & lymphatic drainage networks associated with the primary tumor frequently  determine the pattern of metastasis Discuss patterns of metastasis  Invasion or local spread is a prerequisite for metastasis  In its earliest stages, local invasion may occur by direct tumor extension  Cells migrate away from the primary tumor & invade surrounding tissue  Colon cancers are spread to the liver by anatomic patterns of lymphatic & venous blood flow  Liver cancers spread through the portal vein to the lungs  Lung cancers spread through the systemic circulation to the brain  Breast cancer spreads through the lymphatics to axillary lymph nodes  Cancers often spread through the lymphatics & then to distant organs through the bloodstream Chapter 6 1. Characterize the three human defensive lines. 1  defense= Innate (natural/native) immunity nd 2  defense= Inflammation 3  defense= Adaptive (acquired) 2. Describe the first line of defense  Form barriers at the body’s surfaces and are in place at birth tp prevent damage  by substances in the environment  Surface barriers  also have microbes known as “normal flora” that can protect us  from pathogens  Physical, mechanical, & biochemical innate natural barriers  Physical: skin tightly epithelial cells & linings of GI, genitourinary & respiratory  tracts               May be sloughed off with dead skin cells that are replaced & expelled  by coughing, sneezing, vomiting, mucus or flushed through urine  Epithelial cells secrete chemical barriers: tears, saliva, ear wax, sweat &  mucus; can trap potential invaders & kills microbes  Antimicrobial peptides kill or inhibit growth of disease causing bacteria,  fungi, & viruses  EX: normal bacteria flora on skin Staphylococcus aureus  Prolonged antibiotic treatment can diminish colonization of normal microbiome,  decreasing its protective activity, and lead to an overgrowth of pathogenic  microorganisms  Opportunistic pathogens= cause disease if the individual’s defenses are  compromised 3. Describe the second line of defense; diagramming the sequence and  consequences of the acute inflammatory process. Inflammatory response:  occurs in tissues with blood supply (vascularized)  activated rapidly after damage  activity by cellular & chemical components  nonspecific= takes place in about the same way regardless of the type of stimulus or whether exposure to the stimulus has occurred  Complement cascade= destroys pathogens directly; classical, alternative, lectin pathways  Coagulation (clotting) cascade= forms a fibrinous meshwork at an injured or inflamed site; prevents spread of infection, framework for repair & healing, forms clot to stop bleeding insoluble protein (fibrin)  Kinin cascade= activates & assists inflammatory cells; primary kinin (bradykinin); causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, & leukocyte chemotaxis 4. Relate complement, clotting and kinin system to inflammation.  All 3 are Plasma Protein Systems  Each consist of multiple proteins found in the blood, usually in inactive forms;  several are enzymes that circulate as proenzymes  Activation in first components results in sequential activation of others, that lead  to biologic function to help protect the individula.k.a cascade  Larger fragment continues cascade by activating the next component  Smaller fragment has potent proinflammatory activities 5. Identify the source and function of major cytokines involved in innate  immunity. Interleukins= produced by macrophages & lymphocytes in response to stimulation of  PRRs  IL­1= proinflammatory cytokine  IL­10= anti­inflammatory cytokine Interferons (IFNs)= protect against viral infections & modulate the inflammatory  response  Type 1 IFN (IFN­alpha & IFN­beta)= produced & released by virally infected  cells in response to viral double­stranded RNA & other viral PAMPS; do not kill  viruses but are secreted & induce antiviral proteins & protection in neighboring  healthy cells  Type 2 IFN (IFN­gamma)  = produced by lymphocytes & activates macrophages,  resulting in increased capacity to kill infectious agents (viruses/bacteria)  microbiocidal Tumor necrosis factor-alpha= secreted by macrophages in response to PAMP & toll- like receptor recognition  Induces fever by acting as an endogenous pyrogen  Increases synthesis of inflammatory serum proteins  Causes muscle wasting (cachexia) & intravascular thrombosis Chemokines= attract leukocytes to site of inflammation; synthesized by many cells (macrophages, fibroblasts, endothelial cells) 6. Describe phagocytosis and identify the phagocytic cells involved. Phagocytosis= process by which a cell ingests & disposes of foreign material;  production of adhesion molecules  Margination (pavementing) adherence of leukocytes (neutrophils) to  endothelial cells  Diapedesis emigration of cells through the endothelial junctions Steps:  Adherence  Engulfment  Phagosome formation  Fusion with lysosomal granules  Destruction of the target 7. Diagram the consequences of the acute inflammatory process.   Mast cell degranulation   Activation of 3 Plasma Protein systems   Release of subcellular components from the damaged cells   Self­limitin  continues only until the threat of the host is eliminated  The 3 plasma systems are interdependent, resulting in the induction of the other  2  Results in: Vasodilation (increased size of blood cells) increases blood flow to  site. EX: erythema & warmth  Increased vascular permeability (blood vessels become porous) EX: edema  Cellular infiltration (leakage of fluid/exudate; pus)  Thrombosis (clots)  Stimulation of nerve endings (pain)  Vascular changes deliver leukocytes (neutrophils), plasma proteins, &  biochemical mediators to site of injury & act in concert  Heat, swelling, redness, pain 8. Diagram the consequences of the chronic inflammatory process.   Inflammation lasting 2 weeks or longer  Often related to an unsuccessful acute inflammatory response  Can be caused by: high lipid & wax content of a microorganism  Ability to survive inside the macrophage  Toxins, physical irritants, chemicals, particulate matter Persistence of infection, antigens, or foreign body leads to: 1. Persistent acute inflammation 2. Neutrophil degranulation & death 3. Lymphocyte activation 4. Fibroblast activation  All 4 lead to lymphocyte & monocyte/macrophage infiltration (pus)  Tissue repair (scar) 9. Characterize the third line of defense in the human body Adaptive acquired immunity:   Humoral & Cellular immunity   Active & Passive immunity  Humoral= antibodies (immunoglobulins bind to anitgens)  Cellular= T lymphocytes  Immune response= collaboration of B & T cells  Clonal diversity= production of billions of B & T cells before birth that have the  capacity to recognize almost any foreign antigen; occurs in lymphoid organs; B  cells are in the bone marrow & T cells are in the thymus  Clonal selection= to initiate immune response, most antigens must be  processed & presented to the immune cells in a specific manner; antigens are  processed by APCs to present T helper cells  The antigen “selects” those B & T cells with compatible antigen receptors  resulting in only a small population of T & B cells undergo the process  T lymphocyte functions  Active immunity= exposure to antigen, natural  Passive immunity= preformed antibodies T cells are administered mother to  fetus 10.Compare innate immunity with adaptive immunity.  Inflammation is the first responder that contains the initial injury & slows the  spread of infection; whereas adaptive immunity slowly augments the initial  defenses against infection & provides long­term security against reinfection  Innate immunity is activated immediately after tissue damage;  nonspecificsimilar regardless of what caused the tissue damage or if it was  sterile; mediators of inflammation must be removed quickly to limit damage to  other healthy tissue & allow healing; recurrent tissue damage & infection is  identical  Adaptive immunity is inducible; develops more slowly; specific; long­lived &  systemic providing long­term protection  against specific infections; has  memory Adaptive immunity purpose= destruction of infectious microorganism that are  resistant to inflammation; long­term highly effective protection against future exposure  to the same microorganism  Inducible 11. Diagram the interrelationship between humoral and cell­mediated immunity. Humoral= antibodies circulate in the blood & defend against extracellular microbes &  microbial toxin  B cells are responsible for humoral immunity that’s mediated by circulating  antibodies (Igs) Cell mediated= effector T cells are found in the blood & tissues & defend against  intracellular pathogens (viruses) & cancer cells  T cells are responsible for cell­mediated immunity  Acquired active immunity develops in response to antigen; long­lived  Passive immunity performed antibody or lymphocytes may be administered to  people; temporary **All immunogens are antigens but not all antigens are immunogens** 12. Diagram the interaction between lymphocytes and phagocytes.  Phagocytes are found in the bloodstream & protect the body by ingesting & destroying foreign cells such as bacteria, viruses, & invading cells; receptors  on phagocytes detect foreign cells & engulf/destroy them  Lymphocytes release antibodies (T & B , NK cells) which destroy microbes, while  phagocytes engulf and digest them phagocytes also have a lobed nucleus and are  bigger than lymphocytes, which have one big nucleus; B & T cells are involved in the  production of memory cells ***Both are part of the immune system & help to neutralize pathogens**


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