Principles of disease
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| What is neoplasia? | abnormality in cellular differentiation, maturation and control of growth
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| What is cell proliferation and what controls it? | time in which cells pass through cell cycle . controlled by cyclins and growth factors such as EGF, PDGF, IGF, fibrolast GF, interleukins and hormones.
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| What is hyperplasia? | proliferation of cells beyond the amount normally seen if cells are capable of dividing. May be seen in hypertrophy.
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| What does physiologic hyperplasia include? | hormonal hyperplasia - proliferation of glandular epithelium of breasts; compensatory hyperplasia - portion of tissue is removed or diseased (as in mitotic restoration of liver)
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| What does pathologic hyperplasia result from? | nonphysiological response. excessive hormonal or growth factor stimulus as in uterine epithelial proliferation after menstruation. are at an increased risk of neoplastic transformation
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| What is hypertrophy? | increase in the size of cells resulting in an increase in the size of the organ. can be physiologic or pathologic. only adaptation that can occur in permanent cells
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| What is atrophy? | shrinkage in the size of cell by the loss of cell substance. diminished but not dead. reduction in structural components of cell due to decreased synthesis and increased catabolism or both.
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| What causes atrophy? | lack of use of muscles, denervation caused by lack of stimulation of muscle fibres by lower neurons, lack of trophic hormones, ischemia, aging - senile atrophy.
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| What is metaplasia? | normal mature cells are replaced by another type of mature cell which is normal for that site. ex. squamous cells in smokers lungs replace normal tissue to withstand stress of smoking better
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| What is dysplasia? | disorderly non-neoplastic proliferation. abnormality of both differentiation and maturation, primarily seen in epithelial cells.
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| What is dysplasia characterized by? | nuclear & cytoplasmic abnormalities, increased rate of multiplication, disorderly maturation, loss in uniformity of individual cells and disruption of their normal architecture
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| How does dysplasia differ from neoplasia? | dysplastic lesions are not invasive and may revert to normal
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| How are cancer cells different from normal cells? | self-sufficiency in growth signals, insensitive to growth-inhibitory signals, evasion of apoptosis, limitless replication potential, develop sustained angiogenesis, can invade & metastasize, genomic instability from defecst in DNA repair
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| What are the key points of carcinogenesis? | nonlethal genetic damage is central to, genetic damage may be acquired (enviro) or may be inherited, three classes of normal principal targets of damage
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| What are the principal targets of carcinogenesis? | growth-promoting protooncogenes, antioncogenes, genes that regulate apoptosis, and genes that regulate DNA repair also play an important role.
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| What does self-sufficiency in growth signals mean? | activation of specific DNA sequences known as protooncogenes leads to promotion of cell growth, without the need for normal growth-promoting signals
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| What are the steps behind protooncogene mutation? | protooncogenes mutate into oncogenes and produce oncoproteins that promote cell growth
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| What can oncogenes code for? | growth factors, growth factor receptors (over-expression), signal-transducing proteins, nuclear trancription factors, cyclins and cyclin dependent kinases (all 3 lead to continuous proliferation)
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| What causes insensitivity to growth inhibitory signals? | tumor suppressor genes are disrupted or mutations of molecules which normally act to inhibit cell proliferation - commonly P53
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| What is P53? | Tumor suppressor gene that is commonly mutated. has anti-proliferative effects (activates quiescence) and regulates apoptosis. Also manages DNA-damage response and monitors for stress in the cell.
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| What causes limitless potential for replication? | telomeres regulate normal lifespan of cells by shortening beyond a certain point that they can no longer divide. Tumor cells activate telomerase and allow cells to replicate indefinitely.
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| What are the steps needed for a cell to metastasize? | intercellular junctions loosen between tumor cells, attachment to and degradation of basement membranes and ECF, locomotion through degraded membranes, extravasation, metastatic deposit, angiogenesis and growth
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| What is meant by multistep carcinogenesis? | cancer progression results from the accumulation of multiple mutations. Tumor cells are less sensitive to immune response and therapy.
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| How is tumor response related to heterogeneity? | multiple mutations produce subclones which have fitness, many different factors work together to evolve into a resistant cell
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| What type of agents can cause neoplasia? | cause of most cancers is unknown and are of multifactorial origin. some substances that play a role in cancer include carcinogens (chemicals, radiation & viruses) hormones, genetic factors, environment and chronic irritation.
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| How long does it take for a carcinogen to produce cancer? | latent period between time of exposure and time of tumor development is variable but may be as long as several decades
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| How do chemical carcinogens function? | they are highly reactive electrophiles which react with electron-rich atoms in nucleic acid and cellular proteins
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| What are direct acting carcinogens? | weak carcinogens that do not require metabolic conversion.
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| What are indirect acting carcinogens? | they are not active until converted to an ultimate carcinogen by endogenous metabolic pathways
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| What is the initiation-promotion sequence? | exposure to the initiator (mutagenic chemical) is followed by exposure to the promoter that augments the carcinogenicity of the initiator.
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| What are the four major histologic types of lung carcinomas? | squamous cell carcinoma, adenocarcinoma, small-cell carcinoma and large-cell carcinoma - SCC is not curable by surgery because it will have already metastasized by the time of diagnosis
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| What clinical signs are associated with bronchogenic carcinomas? | firm gray-white mucosal lesions, intraluminal masses that invade bronchial mucosa or form bulky masses that push into adjacent parenchyma, some masses undergo cavitation, necrosis and hemorrhage and some may extend to pleural cavity
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| What aids can be used to diagnose lung cancer? | examination of sputum, bronchoscopy and radiographs
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| What effects does radiation have on the body? | chromosome breakage, translocations, and point mutations. Non-lethal doses may induce genomic instability which favors carcinogenesis.
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| What are oncogenic viruses? | DNA viruses. papillomavirus (carvical cancer), epstein-barr virus (nasopharyngeal carcinoma, Burkitt's lymphoma as well as other lymphomas in AIDS patients), hepatitis B virus (hepatocellular carcinoma)
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| What are retroviruses? | oncogenic RNA viruses. known to cause cancer in animals. cause neoplastic transformation by acute transformation viruses containing viral oncogene (v-onc) and slow transforming viruses insert their DNA near a cellular oncogene
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| What is helicobactor pylori? | linked to pathogenesis of gastric epithelial cancers and gastric B-cell lymphomas.
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| How are tumours classified? | by their site, biologic behaviour, tissue of origin, or appearance
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| What is the biologic behaviour of benign tumours? | they grow slowly, are noninvasive, do not metastasize. usually encapsulated and excision can be curative.
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| What is the biologic behaviour of malignant tumours? | grow rapidly, behave invasively and metastasize to other parts of the body without any clear boundaries. life-threatening.
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| How can you determine if a tumour is benign or malignant? | differentiation of parenchymal cells and anaplasia (malignant). Well-differentiated cells resemble normal tissue type and are usually benign.
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| What do anaplastic cells show? | pleomorphism (anisokaryosis, anisocytosis), increased nuclear size relative to cell size, hyperchromatic nuclei, chromatin is coarse/clumped, multinucleated giant cells, mitoses numerous & atypical. not recognizable as cell of origin
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| What are the three pathways that cancers disseminate by? | seeding within body cavities (neoplasms), lymphatic spread (typical of carcinomas and melanomas), hematogenous spread (favoured by sarcomas)
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| How are tumours from differentiated cells named? | by their tissue origin. divided into epithelial and mesenchymal types. benign epithelial is an adenoma if from a gland and papilloma if from surface. benign mesenchymal tumours have suffix -oma after cell type of origin and malignant have -sarcoma
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| What is paraneoplastic syndrome? | clinical effects produced by cancer which are unrelated to the direct involvement of the tissue by the tumour. include anemia, immunodeficiency, myopathy, neuropathy, hypercalcemia, cahexia
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| How is cancer staging determined? | The TNM system (tumour, lymph nodes, metastases) classifies the tumour based on size and appearance of the primary tumour.
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| What are the categories of cancer therapy? | surgical removal, radiation therapy, chemotherapy, and immunotherapy
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| How does chemotherapy affect cells? | interferes with cell metabolism and RNA or protein synthesis, blocks DNA replication or mitotic division, exerts hormonal effects
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| What is agenesis? | failure of development of the anlage in the embryo, resulting in complete absence of the organ
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| What is dysgenesis? | abnormal differentiation of an organ anlage, leading to an abnormally formed organ
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| What is hypoplasia? | if organ anlage differentiates properly but growth stops too soon, small but structurally normal organ results
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| What is congenital disease? | disease which is present at birth, regardless of causation
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| What are teratogens? | agents which cause congenital malformations. fetus is most sensitive to them during organogenesis. can be infections, chemicals or radiation.
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| What are the categories of inherited disease? | chromosomal disorders, single gene disorders and polygenic or multifactorial disease
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| What do chromosal disorders result from? | abnormalities in the chromosomal structure or number.
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| What is nondisjunction? | homologous chromosomes fail to separate during the first meiotic division
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| What does aneuploid mean? | having a chromosome number which is not an exact multiple of the normal haploid number (humans=23)
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| What is Klinefelter syndrome? | male hypogonadism resulting from nondisjunction of sex chromosomes, usually 47 XXY. also can result in increased length from soles to pubic bone, reduced facial/body hair, often sterile.
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| What is Turner syndrome? | Monosomy of the short arm of the X chromosome results in hypogonadism in females. results in 45 X karyotype. includes short stature, lyphoedema, broad chest, low hairline, low-set ears, webbed neck, amenorrhea, poorly developed sex characteristics.
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| What is fragile X syndrome? | unusually large number of repeat nucleotide triplets close to the tip of the long arm of the X chromosome.
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| What are the characteristics of Down syndrome? | trisomy of chromosome 21. features include Simian crease, almond shaped eyes, shorter limbs, poor muscle tone. clinical concerns include congenital heart defects, GI abnormalities, cognitive defects. shorter life expectancy.
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| What is Edwards syndrome? | trisomy 18. severe mental retardation and physical defects. low survival rate after one year.
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| What is Patau syndrome? | trisomy 13. abnormal development of the forebrain and midline facial structures. most die soon after birth
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| What is mosaicism? | when two chromatids fail to divide, it is the presence of two or more genetically different cell populations in the same individual
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| What is deletion? | when a portion of a chromosome is lost
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| What is translocation? | transfer of one part of a chromosome to another
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| What does Mendelian disorder refer to? | single gene defects resulting from a mutation in a single gene, inherited in a Mendelian fashion. classified by pattern of inheritance: dominant, recessive, sex-linked
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| What does pleitropy refer to? | the many phenotypic effects a single-gene mutation can lead to
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| What are the characteristics of an autosomal dominant disorder? | both parents affected/carriers, new mutations can cause disorder without parents being affected, reduced penetrance or variable expressivity possible
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| What are the characteristics of autosomal recessive disorders? | both parents of affected child can be symptomless carriers, complete penetrance common, enzyme proteins affected by mutation. occur most frequently in restricted populations.
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| What are sex-linked disorders? | linked to the X chromosome. affected males do not pass on to sons but all daughters are carriers.
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| What are inborn errors of metabolism? | single-gene abnormality that causes failure of synthesis of a specific enzyme. lack of the critical enzyme causes interruption of a biochemical pathway. the substrate of the reaction will accumulate abnormally, leading to a deficiency in the product.
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| What is phenylketonuria? | inborn error of metabolism. phenylalanine hydroxylase is absent, preventing conversion of phenylalanine to tyrosine. Phe is toxic to nerve cells and causes mental retardation.
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| What is a lysosomal storage disease? | lack of lysosomal enzyme contributes to incomplete catabolism of accumulation of these insoluble metabolites withing lysosomes. very rare, includes tay-sachs disease, Nemann-Pick disease and Gaucher disease
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| What is glycogen storage disease? | defect in one of the enzymes involved in glycogen synthesis or breakdown leads to excessive accumulation or abnormal form of glycogen
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| What is Marfan syndrome? | abnormal formation of glycoprotein, fibrillin 1, affects microfibrils in ECM and affects all tissues. related to defects in skeletal, ocular and cardiovascular system.
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| What are Ehlers-Danlos syndromes? | defects in collagen synthesis or structure. skin is hyperextensible and fragile
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| What is familial hypercholesterolemia? | mutation in receptor protein which codes for LDL. inherited in autosomal dominant fashion. impaired intracellular transport and catabolism of LDL and accumulation in the plasma.
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| What happens when proteins that regulate cell growth are mutated? | mutations of protooncogenes and cancer suppressor genes are central to carcinogenesis.
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| What are multifactorial disorders? | disorders that are caused by many factors (ex. genetic plus environmental). includes atherosclerosis, diabetes mellitus, hypertension
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| What is a "threshold effect"? | disorder manifests only when a certain number of effector genes, as well as conditional, environmental influences are involved.
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| What are the mechanisms behind diabetes mellitus? | deficiency of insulin leads to elevated glucose levels in blood and inability of body's cells to utilize glucose.
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| What are the methods used to diagnose genetic diseases? | genetic screening for risk of passing on inherited disease, amniocentesis, karyotyping and FISH. molecular detection can also be used - PCR amplifies DNA/RNA and linkage analysis is used when implicated gene is not known.
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| What is fatty degeneration? | triglyceride accumulates in cytoplasm of parenchymal cells
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| What is fatty liver degeneration? | fatty accumulation in liver due to increased mobilization of adipose tissue, overactivity of certain enzyme systems, oxidation of triglycerides to other forms decreased, apoprotein synthesis decreased
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| What is local hemosiderosis caused by? | local accumulation of iron when hemoglobin is broken down at sites of hemorrhage. contusions
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| What is jaundice and its mechanisms? | jaundice is an increase in serum bilirubin. can be caused by RBC broken down in large numbers - increases bilirubin (hemolytic), liver injured - conjugation of bilirubin affected (hepatocellular), biliary tract obstructed (obstructive)
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| Define necrosis and the cytoplasmic and nuclear signs. | cell is damaged past point of no return. cytoplasm deeply staining and vacuolated, autolysis (fuzzy), nuclear chromatin clumps, nucleus pyknotic and/or karrhyorhexis or karrhyolysis occurs
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| What is the gross evidence of necrosis? | coagulation (pale, dry demarcated areas), liquefaction (liquid, creamy yellow pus), caseous (cheese-like), fat (white chalky deposits)
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| What are the problems associated with necrosis (clinical signs)? | altered function of cells (stroke, heart attack), gangrene (caused by ishcemia - dry or wet), secondary bacterial infection, systemic effects (fever and increased white BC), local effects, release of enzymes from necrotic cells into blood
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| What changes occur post-mortem? | rigor mortis (ATP), post mortem lividity, blood clotting (heart), putrefaction results, autolysis
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| What causes localized edema? | results from localized disturbance of fluid exchange mechanism in the tissue. important venous obstruction (fluid remains in tissue), lymphatic obstruction (osmotic pressure causes fluid to remain in tissue), acute inflammation & acute allergic rxn
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| What causes generalized edema? | congestive heart failure affects the pumping of the heart, venous blood backs up. increased pulmonary venous hydrostatic pressure, fluid moves into alveolar spaces = pulmonary edema
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| How do sodium and water retention exacerbate generalized edema? | in heart failure, glomerular filtration pressure in kidney decreases which stimulate renin which leads to increased aldosterone. this increases Na resorption and water retention in DT of kidney, adding to edema
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| What is hyperproteinemia? | second major cause of generalized edema. low levels of serum protein decrease plasma osmotic pressure and fluid remains in tissue spaces. decreases overall plasma volume.
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| What is the difference between lethal and non-lethal cell injury? | non-lethal is degeneration, can operate at sub-maximal level and can be reversed. Lethal cell injury is the point of no return, leads to necrosis.
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| What is apoptosis? | programmed cell death
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| Outline the four basic mechanisms of cell degeneration and necrosis. | ATP inhibition, impaired cell membrane function, cellular accumulation and genetic abnormalities. Damage cells to the point that they can no longer function.
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| Outline the causes of and describe the outcomes of impaired cellular energy production | caused by hypoxia, enzyme inhibition, hypoglycemia, uncoupling of oxidative phosphorylation. leads to accumulation of H2O and Na, swelling of mito, switch to anaerobic metabolism (pH decreases)
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| How are DNA abnormalities manifested at a cellular level? | interference with mitosis, failure of synthesis of structural proteins, failure of growth-regulating proteins, failure of enzyme synthesis
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| What are some of the clinical side effects of edema? | puffy swelling, right ventricular failure causes back up of venous blood (systemic edema), left heart failure causes increased venous hydrostatic pressure and build up of fluid in lungs.
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| What is effusion? | fluid accumulates in body cavities
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| What is ascites? | effusion in the peritoneal cavity
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| What is anasarca? | massive edema of whole body
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| What causes hemorrhage and what are some clinical signs? | trauma to vasculature, atherosclerosis, inflammation of vessel wall. Petichiae is pinpoint, purpura are small oval shaped, ecchymoses are bruises, hematoma is a "blood blister"
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| What is fibrinolysis? | fibrin formed to clot is broken down by plasmin, controls clotting
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| What are the three major causes of thrombosis? | clotting within a vessel - Virchow triad: endothelial injury, stasis of turbulence of blood flow, blood hypercoagulability
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| What is atherosclerosis and associated complications? | build up of plaque in arteries - interference of blood supply to heart, brain, extremities, compromise to smaller arteries causing ischemic injury, aneurysm, embolism
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| What is an embolism and its effects? | free-floating intravascular solid, liquid or gaseous mass - blocks lumen of artery impeding blood flow to tissue - depends on size, circulatory arrangements, vulnerability of tissue
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| Outline the effects of ischemia. | failure of blood supply to tissue - causes infarct
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| Define infarction and outline its pathogenesis. | localized area of necrosis resulting from inadequate blood supply - functional changes in tissue, pain
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| What are the factors influencing the outcome of arterial and venous obstruction? | coronary artery (pale) - myocardial infarction, venous obstruction (red) - stasis
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| Define disseminated intravascular coagulation. | thrombohemorrhagic disorder resulting from triggered by endothelial cell injury and release of tissue factor - activation of coagulation: leads to sepsis, endothelial injury, obstetric complications, neoplasms, massive tissue injury
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| Define shock and its complications. | reduced tissue perfusion leading to reduction in cardiac output or circulating blood volume: hypervolemia - loss of fluid; peripheral vasodilation; cardiogenic shock - failure of heart to function as pump
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| Describe how body compensates for shock and how shock becomes irreversible. | nonprogressive - heart beats more rapidly, peripheral vasoconstriction: leads to progressive with extended vasoconstriction (tissue hypoxia)
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| Name the cardinal signs of inflammation. | redness, heat, swelling, pain
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| describe the role of the acute inflammatory response. | first line of defense in injury
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| describe the acute inflammatory response in terms of vasculature changes and cellular response. | vessels become dilated (redness) and leaky (swelling). Emigration of inflammatory cells (white BC) from blood to area of tissue injury.
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| How does inflammatory exudate form? | widening of spaces in endothelial cells causes an increased movement of fluid and larger molecules out of vasculature and into cells. Fluid that forms in tissues called exudate.
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| What is the difference between exudate and transudate? | Exudate is composed of proteins, cells as well as blood. Transudate is composed of ultrafiltrate.
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| What is the difference between granulocytes and mononuclear cells? | granulocytes (neutrophils, basophils, eosinophils) have the greatest role in inflammation. mononuclear (lymphocytes, plasma cells, monocytes, macrophages) have a greater role in later more chronic stages.
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| How do inflammatory cells reach the site of inflammation? | margination, rolling and adhesion of leucocytes (selectins "sticky"). Emigration of neutrophils (diapedesis squeeze between junctions) Chemotaxis. Leucocyte activation & phagocytosis (Opsonization)
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| What is the role of chemical mediators in inflammation? | inactive precursors that are activated by enzymes, bind to specific receptors to release further mediators. vasoactive amines, plasma proteases, lysosomal constituents, arachidonic acid metabolism, platelet-activating factor, cytokines
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| What are the signs of acute inflammation? | pain, fever, malaise, changes in peripheral white BC count and changes in plasma proteins
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| What are the possible outcomes of acute inflammation? | resolution, repair, regeneration or scar formation, suppurative inflammation which can lead to abscess
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| What is septicemia? | refers to the spread of bacteria and their toxins via the bloodstream
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| What causes fever? | pyrogens
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| What are some nonspecific defense mechanisms? | physical barrier, lysozyme, digestive enzymes
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| What characterizes the immune response? | specificity to antigens, memory of antigens and an enhanced response to a second exposure of the same antigen
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| what is an antigen? | molecules which evoke an immune response when introduced into a host. extrinsic are foreign, intrinsic are components of the body
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| Describe the concept of self-tolerance. | lack of response to our own antigens
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| Define the terms T and B cells. | They are lymphocytes. T cells transform into effector or helper cells, B cells transform into antibody-producing plasma cells
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| What are the major functions of macrophages in in the immune response? | phagocytosis, act as filters, sentinels to alert B and T cells
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| What so effector T cells do? | cell mediated immunity (kills cells with a surface antigen), helper roles (produce cytokines)
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| What are the five immunoglobulin classes? | IgG - opsonize target cells, IgA - neutralize microbes in lumen of respiratory and GI tracts, IgE - coat helminths and function w/ mast cells & eosinophils to kill the parasites, IgD - on B cell receptor with IgM
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| Describe antibody production by B cells. | differentiate into plasma cells to make Ab specific to Ag
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| Describe how passive immunity is naturally acquired. | through colostrum
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| Describe function of lymph nodes. | Ag may be carried first to lymph nodes where they are exposed to a large amount of macrophages and lymphocytes. T cells and B cells transform
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| What are the mechanisms inittiated by Ag-Ab interactions? | agglutination, opsonization, complement fixation
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| What is the primary and secondary response? | first exposure to antigen has a lag period when B cells produced with specific receptors for Ag, IgM produced first and IgG produced later. 2dary response is faster and produces IgG first due to memory cells
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| What is passive immunity? | pre-formed Ab transferred from another person
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| What is active immunity? | vaccination
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| What are the factors in the outcome of tissue transplantation? | histocompatibility (Ag-specific T cells, HLA Ag, MHC). T-cell mediated rejection and Ab-mediated rejection. Hyperacute rejection is when Ab is present in host before transplant, response is immediate
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| How does HIV cause AIDS? | HIV affects T cells, macrophages and dendritic cells. T cells very low, once diminished - AIDS
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