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Patho Midterm 1

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Question
Answer
pathophysiology   the study of the underlying changes in body physiology that results from or is caused by disease or injury.  
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etiology   cause of disease  
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idiopathic   disease of unknown cause  
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iatrogenic   disease as a result of medical/surgical treatment  
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nosocomial   disease that results from being in a hospital environment  
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diagnosis   naming or identification of a disease  
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clinical manifestations   evidence of disease  
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sign   objective alterations that can be observed or measured by another person  
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symptom   subjective experience by the patient  
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prognosis   expected outcome of a disease  
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acute disease   sudden appearance of signs or symptoms of disease(short time period)  
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chronic disease   slow development, long time period of signs or symptoms of disease  
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remissions   periods when symptoms disappear or diminsh significantly  
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exacerbations   periods when symptoms are much worse/severe  
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complication   onset of another disease in a person who is already coping with a pre-existing disease  
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sequelae   unwanted outcomes of having disease or result of trauma  
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prodrome/prodromal period   time(usually at illness start) when patient has vague symptoms before onset of specific disease signs and symptoms  
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insidious   slow, vague, nonspecific feelings of change in the body  
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latent period   time during which no symptoms are apparent, but disease is present  
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syndrome   group of symptoms and/or signs that occur together that may be caused by interrelated problems or a specific disease  
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disorder   abnormality of function  
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risk factors/predisposing factors   increase probability that disease will occur (but are not causes)  
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precipitating factor   a condition or event that causes a pathologic event or disorder  
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purpose of DNA   synthesis of proteins- genetic code  
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mutation   any alteration of genetic material  
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pyrimidines   cytosine and thymine  
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purines   adenine and guanine  
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transcription   RNA is synthesized from the DNA template, results in formation of mRNA, RNA Polymerase binds to promoter and txn continues until termination sequence  
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translation   process by which RNA directs the synthesis of a polypeptide  
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Chromosomes   condensed DNA and protein(chromatin) into dark staining organelles. Contain genes  
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genes   basic units of inheritance  
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somatic cells   all cells besides gametes. Contain 46 chromosomes(23 pairs). Diploid Cells  
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Gametes   sperm and egg cells. Contain 23 chromosomes. Haploid Cells. Contain one member of each chromosome pair  
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autosomes   the first 22 of the 23 pairs of chromosomes in males and females. Homologous  
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Homologous Chromosomes   identical chromosomes  
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sex chromosomes   remaining pair of chromosomes(23rd pair). In females it is XX and in males it is XY  
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karyotype   ordered display of chromosomes  
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Euploid Cells   have a multiple of the normal number of chromosomes  
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Polyploid Cell   when a euploid cell has more than the diploid number  
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Triploidy   a zygote having 3 copies of each chromosome (69 total) - polyploid  
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tetraploidy   a zygote having 4 copies of each chromosome (92 total)- polyploid  
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aneuploidy   a somatic cell that does not contain a multiple of 23 chromosomes  
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Trisomy   a cell containing 3 copies of one chromosome  
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monosomy   presence of only one copy of any chromosome (lethal)  
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nondisjunction   Failure of homologous chromosomes or sister chromatids to seperate normally during meiosis or mitosis. Usually the cause of aneuploidy  
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partial trisomy   only an extra portion of a chromosome is present in each cell  
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chromosomal mosaics   trisomies occurring only in some cells of the body  
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Down Syndrome   Trisomy 21. Mentally retarded, low nasal bridge, epicanthal folds, protruding tongue, poor muscle tone  
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Trisomy X   female that has 3 X chromosomes. "Metafemales". Variable symptoms: sterility, menstrual irregularity, mental retardation  
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Turner Syndrome   females with only one X chromosome. Absence of ovaries, sterile, short stature, webbed neck. edema, underdeveloped breasts, wide nipples, usually inherited from mother  
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Klinefelter Syndrome   At least 2 X's and one Y. Can be XXY or XXXY. Male appearance, female like breasts, small testes, sparse body hair, long limbs  
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Cri du Chat Syndrome   rare genetic disorder. Deletion of short arm of chromosome 5. Low birth weight, mental retardation, microcephaly  
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deletions   broken chromosomes and lost DNA  
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fragile sites   areas on chromosomes that develop distinctive breaks or gaps when cells are cultured  
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fragile X syndrome   fragile site on long arm of the X chromosome. Associated with mental retardation. Higher incidence in males b/c they dont have another X to compensate. Females can be carriers. Caused by CGG repeats  
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genetics   mechanisms by which an individuals set of paired chromosomes produces traits  
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locus   position of a gene along a chromosome  
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allele   a different form of a particular gene at a given locus  
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homozygous   loci on a pair of chromosomes have identical genes/alleles  
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heterozygous   loci on a pair of chromosomes have different genes/alleles  
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genotype   the genetic makeup of an organism. "What the have"  
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phenotype   the observable, detectable, or outward appearance of the genetics of an organism. "What they demonstrate"  
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dominant allele   Allele with observable effects in a heterozygote. Capital Letter  
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recessive allele   Allele with hidden effects in a heterozygote. Lowercase Letter.  
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carrier   an individual who has a disease gene but is phenotypically normal  
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pedigrees   summarizes family relationships and shows which members of a family are affected by a genetic disease  
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proband   first person in the family diagnosed or seen in a clinic  
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autosomal dominant disorder   abnormal allele is dominant, normal allele is recessive, and the genes exist on a pair of autosomes  
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recurrence risk   the probability that parents of a child with a genetic disease will have yet another child with the same disease. Same for each subsequent child  
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penetrance   the percentage of individuals with a specific genotype who also express the expected phenotype  
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expressivity   variation in a phenotype associated with a particular genotype  
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autosomal recessive disorder   abnormal allele is recesssive and a person must be homozygous for the abnormal trait to express the disease  
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Sex Linked(X-linked) disorders   usually expressed in males because females have other X to mask abnormal gene. Recessive. Males have only one X chromosome so they are hemizygous for genes on the X chromosome. If they inherit a recessive gene, on Xm he will be affected  
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polygenic   variation in traits caused by the effects of multiple genes  
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multifactorial trait   variation in traits caused by genetic and environmental or lifestyle factors  
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quantitative traits   traits that are measured on a continuous numeric scale  
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5 types of adaptations   atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia  
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atrophy   decrease or shrinkage in cellular size(can lead to entire organ shrinkage). Most common in skeletal muscle, heart, secondary sex organs, brain.  
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physiologic atrophy   occurs with early development (ex. thymus glad during childhood)  
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pathologic atrophy   occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormones, and nervous stimulation  
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hypertrophy   increase in size of cells (and affected organ); most common in heart and kidneys. Due to protein accumulation  
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triggers for hypertrophy   1) Mechanical- stretch 2) Trophic- growth factors, hormones, vasoactive agents  
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physiologic hypertrophy   occurs in response to heavy work; diminishes with lighter workload. Occurs when kidney adapts to removal of part of damaged kidney and during pregnancy with mammary glands and uterus  
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pathologic hypertrophy   example is in the heart due to hypertension  
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hyperplasia   increase in number of cells resulting form an increased rate of cellular division  
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Compensatory Hyperplasia (Physiologic)   enables certain organs to regenerate . example is regeneration of liver cells.  
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Hormonal Hyperplasia(Physiologic)   occurs chiefly in estrogen dependent organs such as uterus and breast. Hyperplasia(along with hypertrophy) allows these to enlarge.  
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Pathologic Hyperplasia   abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or growth factors on target cells  
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dysplasia   abnormal changes in the size, shape, and organization of mature cells; not a true adaptive process, often occurs in epithelial tissue of the cervix and respiratory tract  
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metaplasia   reversible replacement of one mature cell type by another, sometimes less differentiated cell type.  
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cellular injury   occurs if the cell is unable to maintain homeostasis. Can be reversible/recovery or irreversible/death.  
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4 common biochemical themes of cell injury   ATP depletion, oxygen and oxygen-derived free radicals, calcium alterations, defects in membrane permeability  
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ATP depletion   loss of mitochondrial ATP and decreased ATP synthesis; results in cellular swelling, decreased protein synthesis, decreased membrane transport, lipogenesis, loss of integrity of plasma membrane  
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Oxygen and Oxygen derived free radicals   lack of oxygen leads to injury, free radicals(O2-,H2O2, OH.) cause destruction of cell membrane/structure  
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Calcium Alterations   normally intracellular Ca concentrations are low; ischemia and chemicals cause an increase in cytosolic Ca++ concentrations. Causes intracellular damage  
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Defects in membrane permeability   early loss of selective membrane permeability is found in all forms of cell injury  
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3 common forms of cell injury   Hypoxia, free radicals/reactive oxygen species injury, chemical injury  
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hypoxia   lack of sufficient oxygen; single most common cause of cell injury  
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ischemia   reduced blood supply, not enough oxygen  
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anoxia   total lack of oxygen  
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Cellular Responses to Hypoxic Injury   decrease in ATP production, increased anaerobic metabolism, decreased glycogen, failure of sodium potassium pump and sodium calcium exchange, cellular swelling vacuolation, damage to membrane  
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Free Radicals/Reactive Oxygen Species Injury (oxidative stress)   occurs when excess ROS overwhelms endogenous antioxidant systems. Cause damage by lipid peroxidation, membrane damage, increased permeability, attacking proteins, fragmenting DNA, and damaging mitochondria  
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free radical   electrically uncharged atom or group of atoms that has an unpaired electron. To stabilize, they give up or steal an electron. When the attacked molecule loses its electron, it becomes a free radical. Hard to control  
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antioxidants   SOD, glutathione peroxidase, catalase, vitamin E. ROS overwhelm them  
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chemical injury   biochemical interaction between toxic substance and the cell's plasma membrane(leads to increased permeability); CCl4, lead, CO, ethanol, mercury, drugs  
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lead   a heavy metal in the environment, hazardous mostly for children and pregnant mothers; affects nervous system, hematopoietic system, and kidneys.  
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effects of lead   Alters calcium, interferes neurotransmitters, inhibits enzymes involved in hemoglobin synthesis, causes anemia, convulsions, delirium, paralysis, nausea, weight loss, etc  
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carbon monoxide   odorless, colorless, undetectable gas produced by incomplete combustion of fuels. Produces hypoxic injury- affinity for hemoglobin is higher than oxygen so oxygen cant bind  
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ethanol   causes nutritional disorders and liver injury  
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4 Unintentional and Intentional Injuries   blunt force injuries, sharp force injuries, gunshot wounds, asphyxial injuries  
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blunt force injuries   application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues  
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contusion   bruise; bleeding into skin or underlying tissues as a result of a blow that squeezes or crushes the soft tissues and ruptures blood vessels without breaking the skin. Color changes (red/purple->blue/black-> yellow/green/brow) reflect healing process  
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hematoma   collection of blood in soft tissue or an enclosed space  
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subdural hematoma   collection of blood between inner surface of dura mater and brain resulting in shearing of small veins that bridge the subdural space  
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epidural hematoma   collection of blood between inner surface of the skull and the dura. Caused by a torn artery  
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abrasion   scrape; results from removal of the superficial layers of skin that was caused by friction between skin and injuring object  
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laceration   tear or rip resulting when the tensile strength of the skin or tissue is exceeded. Jagged or irregular  
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avulsion   wide area of tissue pulled away, creating a large skin flap  
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sharp force injuries   cutting and piercing injuries  
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incised wound   cut that is longer than it is deep. sharp, distinct edges without abrasion  
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stab wounds   a penetrating sharp force injury that is deeper than it is long; depths of wound are clean and distinct, no underlying or associated crush injury; a lot of internal bleeding  
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puncture wounds   caused by instruments or objects with sharp points but without sharp edges  
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chopping wounds   combo of sharp and blunt force; axes, hatchets, etc  
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gunshot wounds   can be penetrating(bullet retained in body) or perforating(bullet exits)  
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contact range entrance wounds   occur when gun is held so the muzzle rests on or presses into the skin surface  
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blowback   occur in hard contact wounds of the head; gas and explosive energy sent into wound causes severe tearing and disruption of tissues, giving the wound a large, gaping and jagged appearance  
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muzzle imprint   patterned abrasion that mirrors the features of the weapon  
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intermediate range entrance wound   surrounded by gunpowder tattooing or stippling  
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indeterminate range entrance wound   occurs when the only thing striking the body is the bullet  
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exit wounds   shape can be round or slit like to completely irregular  
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ashpyxial injuries   caused by failure of cells to receive or use oxygen  
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suffocation   oxygen failing to reach the blood; results from lack of oxygen in environment or blockage of airways. Includes choking asphyxiation- obstruction of internal airways  
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strangulation   caused by compression and closure of the blood vessels and air passages resulting from external pressure on the neck; results in stop of blood flow to brain; hanging, ligature, manual strangulation  
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chemical asphyxiants   cyanide and hydrogen sulfide  
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drowning   alteration of oxygen delivery to tissues resulting from breathing of fluid/water.  
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dry lung drowning   in as many as 15% of drownings, little or no water enters lungs because of vagal nerve mediated laryngospasms  
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Infectious injury   when a microorganism has disease producing potential(can invade and destroy cells, produce toxins and produce hypersensitivity reactions)  
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Immunologic and Inflammatory Injury   cellular membranes are injured by direct contact with cellular and chemical components of the immune and inflammatory responses  
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complement   responsible for many of membrane alterations that occur during immunologic injury (causes leakage of K+ out of cell and rapid influx of water)  
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cellular accumulations(infiltrations)   occur in normal and injured cells;WATER, lipids, carbs, glycogen, proteins, etc  
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cellular swelling   most common degenerative change;caused by shift of extracellular water into cells.(Hypoxia-> decreased ATP->Na and water move into cell and K diffuses out-> increased osmotic pressure->more water moves into cell->vacuolation->ONCOSIS/VACUOLAR DEGENERATION  
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hemosiderin   yellow brown pigment derived from hemoglobin. How iron is stored in tissue cells when iron levels are high.  
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hemosiderin accumulation   accumulates in areas of bruising and hemorrhage and in lungs and spleen after congestion from heart failure. Skin appears red-blue and then lysis of escaped rbcs occurs, causing hemoglobin to be transformed to hemosiderin  
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calcium accumulation   causes cellular calcification- influx of extracellular calcium in injured mitochondria. Also can be caused by excretion of acid which leads to OH- ions which leads to precipitation of calcium hydroxide and hydroxyapatite  
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dystrophic calcification   occurs in dying and dead tissue  
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metastatic calcification   consists of mineral deposits that occur in undamaged normal tissues as a result of hypercalcemia  
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necrosis   cellular death leading to cellular dissolution; the sum of cellular changes after local cell death and the process of cellular self digestion  
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autolysis   process of cellular self digestion known as autodigestion  
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karyolyisis   nuclear dissolution and chromatin lysis  
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pyknosis   nucleus shrinks and becomes a small dense mass of genetic material  
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karyorrhexis   fragmentation of the nucleus into smaller particles or "nuclear dust"  
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4 major types of necrosis + 2 other types   coagulative, liquefactive, caseous, fatty, gangrenous,gas gangrene  
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coagulative necrosis   occurs in kidneys, heart, and adrenal glands; commonly results from hypoxia caused by ischemia or chemical injury,; caused by PROTEIN DENATURATION  
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liquefactive necrosis   commonly results from ischemic injury to neurons and glial cells in the brain. Brain cells are rich in digestive hydrolytic enzymes and lipids. The cells are digested by their own hydrolases. Tissue becomes soft, liquefies, walled off from healthy tissue.  
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caseous necrosis   usually results from tuberculosis pulmonary infection. Combination of coagulative and liquefactive necroses. Tissues resemble clumped cheese  
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fat necrosis   cellular dissolution caused by lipases that occur in the breast, pancreas, and abdominal organs. Necrotic tissue appears opaque and chalk white  
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lipase   break down triglycerides, releasing free fatty acids, which combine with calcium, magnesium and sodium ions, creating soaps(saponification)  
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gangrenous necrosis   death of tissue from sever hypoxic injury (b/c of arteriosclerosis, blockage of arteries) usually in lower leg  
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dry gangrene   usually the result of coagulative necrosis. skin becomes dry and shrinks, color changes to dark brown or black  
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wet gangrene   develops when neutrophils invade site, causing liquefactive necrosis. Ususally occurs in internal organs. Site becomes cold, swollen, black, foul odor,  
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gas gangrene   special type of gangrene caused by infection of injured tissue by Clostridium sp. Death caused by shock  
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Clostridium   anaerobic bacteria that produce hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas to form in muscle soft tissue.  
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apoptosis   "dropping off"; programmed cellular death. Affects scattered, single cells  
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physiologic apoptosis   important in development of body tissue  
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pathologic apoptosis   result of intracellular events or adverse exogenous stimuli (example: viral hepatitis induces apoptosis). Includes increase in apoptosis or the absence of apoptosis(leads to proliferation/accumulation of cells)  
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characteristics of cellular aging   atrophy, decreased function, loss of cells, .  
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tissue and systemic aging   progressive stiffness and rigidity, sarcopenia(loss of skeletal muscle mass and strength)  
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frailty   mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance, falls, fractures, bone density  
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somatic death   death of an entire person. followed by postmortem changes  
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algor mortis   postmortem reduction of body temperature  
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livor mortis   pooling of blood in most dependent/lowest tissues which develop a purple discoloration  
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rigor mortis   without ATP, detachment of myosin from actin is compromised and the muscles remain in a contracted position  
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postmortem autolysis   release of enzymes and lytic dissolution  
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total body water   the sum of fluids within all body compartments  
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intracellular fluid   all the fluid within cells (2/3 of TBW and 40% of body weight)  
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extracellular fluid   all the fluid outside the cells; interstitial fluid and intravascular fluid (1/3 of TBW and 20% of body weight)  
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interstitial fluid   between cells an outside blood vessels(15% of body weight)  
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intravascular fluid   blood plasma(5% of body weight)  
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effect on aging to TBW   elderly have less TBW because of increase adipose tissue/decrease muscle mass, renal decline results in less retention of water and diminished thirst perception leads to dehydration  
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antidiuretic hormone   secreted by the posterior pituitary gland in response to increased osmolality, decreased blood volume, or decreased blood pressure. Increases water retention by the kidney  
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osmoreceptors   stimulated by hyperosmolality. Stimulate thirst and signals posterior pituitary to release ADH  
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baroreceptors   nerve endings that are sensitive to changes in volume and pressure. When there is a decrease in blood volume and blood pressure, they stimulate ADH  
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Sodium   accounts for 90% of the ECF cations. Regulates extracellular osmotic forces and regulates water balance  
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Chloride   the major anion in the ECF and provides electroneutrality in relation to sodium. Passive transport following active transport of sodium. Maintains acidity of gastric secretions  
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aldosterone   a mineralocorticoid secreted form the adrenal cortex that increases the reabsorption of sodium and the secretion of potassium.  
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RAA Mechanism(Renin Angiotensin Aldosterone)   When blood volume and bp are reduced Renin is secreted by kidney, combines with angiotensinogen to make Angiotensin I. Angiotensin I is converted to Angiotensin II in the lungs by ACE. Angiotensin II stimulates vasoconstriction and stimulates aldosterone  
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Atrial Natriuretic Factor   functions in renal elimination of sodium to control sodium and water balance. Blocks the effects of aldosterone. Also reduces blood pressure.  
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Hypovolemia   fluid volume deficit; fluid loss, reduced fluid intake, fluid shift out of vascular space(3rd spacing). Caused by hemmorhage, polyuria, vomiting, diarrhea, fistulas, fever, nasogastric suctioning, etc  
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1 L of water lost is equal to ??? lbs   2.2 lbs is equal to ??? L of water lost  
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detecting dehydration   thirst, poor skin turgor, dry mucous membranes, tachycardia, weak pulse, postural hypotension. shock, decreased urinary output, elevated hematocrit and serum sodium, skin tenting,  
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electrolytes   substances whose molecules dissociate into ions when placed in water  
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simple diffusion   movement of molecules from areas of high concentration to areas of low concentration; requires no external energy.  
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facilitated diffusion   movement of molecules from areas of high concentration to low concentration; combine with a carrier molecule. Passive(requires no external energy)  
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active transport   passage of ions or molecules across a cell membrane by an energy consuming pricess ; takes place against an electrochemical gradient(low-->high). Example: sodium potassium pump  
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osmosis   movement of fluid through a semipermeable membrane; from area of low solute concentration to area of higher solute concentration until equilibrium is reached. Requires no external energy. Stops when conc. differences disappear or hydrostatic pressure inc.  
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osmolality   osmotic force of solute per unit weight of solvent (describes fluids inside the body)  
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osmolarity   total milliosmoles of solute per unit of total volume of solution (describes fluids outside of the body)  
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isotonic/iso-osmolar solutions   have same osmotic pressure as blood (same amount of solutes); Normal Saline (0.9%), Lactated Ringers Solution, 5% dextrose in water(D5W).  
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hypotonic/hypo-osmolar solution   lower osmotic pressure than blood/fewer solutes; 1/2 normal saline(.45% NaCl) or 2.5% dextrose in water (D2.5W)--> fluid moves into cell to compensate  
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hypertonic/hyper-osmolar solution   higher osmotic pressure than blood/more solutes; hypertonic saline (>5% NaCl), 5% dextrose in NS(D5NS) or 5% dextrose in lactated Ringers solution (D5LR).-->fluid moves out of cell to compensate  
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hydrostatic pressure   force within a fluid compartment that pushes water out. "pushes"  
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oncotic pressure (colloidal osmotic pressure)   osmotic pressure from colloids in solution. Wants to keep water inside. "pulls"  
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What pushes water out of capillaries?   capillary hydrostatic pressure and interstitial oncotic pressure  
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What pulls water into capillaries?   plasma oncotic pressure and interstitial hydrostatic pressure  
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filtration   movement of water and solutes by forces of pressure  
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forces favoring filtration   capillary hydrostatic pressure and interstitial oncotic pressure  
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forces favoring reabsorption   plasma oncotic pressure and interstitial hydrostatic pressure  
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edema   accumulation of fluid in the interstitial spaces. Caused by an increase in plasma hydrostatic pressure, lowering of plasma oncotic pressure, increased capillary membrane permeability, and lymphatic channel obstruction.  
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symptoms of edema   weight gain, swelling, puffiness, limited movement of affected joints, pitting of skin when pressed,  
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second spacing   abnormal accumulation of interstitial fluid (edema)  
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third spacing   fluid accumulation trapped and unavailable for functional use (ascites and edema associated with burns)  
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ascites   accumulation of fluid in the peritoneal space  
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hypothalamus   contains osmoreceptors that sense increases in plasma osmolality. Stimulates thirst and ADH release (ADH is syntehsized here)  
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Pituitary region   releases ADH in response to increased plasma osmolality, decrease in blood volume, stress, nausea, nicotine, morphine  
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Syndrome of Inappropriate Antidiuretic Hormone Secretion   occurs when factors other than hyperosmolality or hypovolemia stimulate secretion of ADH. Causes water to be retained in excess (decrease renal excretion of water)  
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Renal Regulation (function of kidneys)   primary organ for regulating fluid and electrolytes, ADH and aldosterone work on its tubules, impairment causes edema, potassium and phosphorus retention, acidosis  
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ways of losing water   vaporization from lungs and skin, increased body temp/exercise, excessive sweating  
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hypovolemia   fluid volume deficit; fluid loss, reduced fluid intake, fluid shift out of vascular space(3rd spacing). Caused by hemmorhage, polyuria, vomiting, diarrhea, fistulas, fever, nasogastric suctioning  
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clinical manifestations of hypovolemia   restlessness, drowsiness, lethargy, confusion, thirst, dry mouth, decreased skin turgor, dizziness, postural hypotension, weakness, weight loss, increased respiratory rate, seizures, coma, etc  
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hypervolemia   fluid volume excess; caused by excessive isotonic/hypotonic IV fluids, renal/heart failure, polydipsia, SIADH, etc.  
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clinical manifestations of hypervolemia   headache, confusion, lethargy, peripheral edema, distended neck veins, bounding pulse, increased BP and CVP, polyuria, muscle spasms, weight gain, seizures, coma  
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osmotic pressure   pressure needed to oppose the movement of water across the membrane  
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Hypernatremia   excess of serum sodium; caused by a loss of water or a gain in sodium intake. Leads to cellular dehydration.  
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Causes of hypernatremia   deficiency in synthesis/release of ADH, decrease in kidney response to ADH, primary aldosteronism, too rapid infusion of hypertonic saline, sodium bicarb, or isotonic saline, drinking salt water, high salt intake, diarrhea, diabetes insipidus, dehydration  
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clinical manifestations of hypernatremia   intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia, etc. Thirst, fever, dry mucous membranes, restlessness  
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Treating Acute Hypernatremia   if it occurs in a period of 48 hours or less, correct it rapidly  
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Treating chronic hypernatremia   corrected more slowly due to risks of brain edema( if extracellular tonicity is decreased to quickly, water will move into brain cells)  
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Hyponatremia   deficit of serum sodium; cause plasma hypo-osmolalty and cellular swelling  
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Dilutional Hyponatremia   occur when proportion of TBW to total body sodium is excessive  
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Hypo-osmolar Hyponatremia   When renal excretion of water is impaired and TBW and sodium are increased, but the retention of water exceeds increase in sodium  
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Hypertonic Hyponatremia   increases in plasma lipids and proteins displace water volume and decrease sodium concentration(hyperglycemia attracts ICF and increase in ECF dilutes concentration of sodium)  
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clinical manifestatins of hyponatremia   decreased osmolality, free water excess, ECF goes into cells and causes hypovolemia, free water excess can also cause hypervolemia/water intoxication; lethargy, confusion, decreased reflexes, seizures, coma  
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causes of hyponatremia   excessive diuresis, excessive sweating, GI loss, adrenocortical insufficiency, excess IV fluids, SIADH  
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Hyperchloremia   excess of chloride, occurs with hypernatremia or deficit in bicarbonate. Manifestations include metabolic acidosis, stupor, deep rapid respirations, weakness, coma  
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hypochloremia   deficit in serum chloride, result of hyponatremia or elevated bicarbonate. Develops as a result of vomiting and loss of HCL. Manifestations include metabolic alkalosis, muscle hypertonicity, depressed respirations, tetany  
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potassium   major intracellular cation. regulates intracellular osmolality, excreted by kidneys, concentration maintained by Na+/K+ pump, regulate intracellular electrical neutrality, essential for action potentials, normal cardiac rhythm, muscle contraction  
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things that affect potassium levels   changes in pH(H+ ions accumulate in ICF during acidosis. K+ shifts out to balance), aldosterone, insulin, epinephrine, alkalosis(all make K+ move into cells)  
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hyperkalemia   elevation of ECF potassium above 5.5 mEq/L.  
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causes of hyperkalemia   increased intake of K+, shift of K+ from the ICF to the ECF, decreased renal secretion, insulin deficiency, or cell trauma  
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ECG changes with hyperkalemia   tall peaked T wave, wide QRS complex, ventricular fibrillation, cardiac arrest  
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clinical manifestations of hyperkalemia   mild: neuromuscular irritability; severe:cell cant repolarize, muscle weakness, loss of muscle tone, flaccid paralysis  
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hypokalemia   decrease in the ECF potassium concentration below 3.5 mEq/L.  
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causes of hypokalemia   reduced intake of potassium, increased intracellular entry of potassium, increased loss of potassium, alcoholism, alkalosis, DIURETICS/ PROLONGED VOMITING/DIARRHEA, aldosterone, laxative abuse, etc.--> K+ shifts from ECF to ICF  
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ECG changes with hypokalemia   flattened T wave, prolonged PR interval, large U wave  
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clinical manifestations of hypokalemia   decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias  
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calcium   essential cation, widely distributed, 99% is found in bone as hydroxyapatite, necessary for bone, clotting, hormone secretions, neuromuscular function, muscle contraction, maintenance of membrane permeability  
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parathyroid hormone   released by low serum Ca2+ (raises Calcium levels in blood--> stimulates bone to release Ca). Also helps excrete phosphate.  
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calcitonin   stimulated by high serum Ca2+(lower calcium levels in blood--> stimulates take up of Ca by bones)  
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vitamin D   reabsorbs Ca2+ from GI tract  
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hypercalcemia   excess of serum calcium. Increases the block of Na+ into cell  
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causes of hypercalcemia   hyperparathyroidism, cancer, vitamin D overdose, hypophosphatemia, thyrotoxicosis, acromegaly, renal failure  
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clinical manifestations of hypercalcemia   decreased neuromuscular excitability, muscle weakness, cardiac arrest, constipation, kidney stones, anorexia, nausea, vomiting, decrease in heart rate, confusion  
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hypocalcemia   deficit of serum calcium. Decreases block of Na+ into cell  
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causes of hypocalcemia   hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, hypoalbuminemia  
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manifestations of hypocalcemia   numbness, muscle crams, increased neuromuscular excitability, weakness, hypotension, Chvostek and Trousseaus signs, tetany, seizures, emotional instability, etc  
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chvostek's sign   contraction of facial muscles in response to light tap over the facial nerve in front of ear  
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trousseau's sign   carpal spasm induced by inflating a blood pressure cuff above systolic pressure for a few minutes  
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Calcium's relationship to Phosphate   inverse relationship; if concentration of one increases, the other decreases  
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phosphate   major intracellular anion, essential to muscle function, RBCs, and nervous system; most is located in bone. Needed for ATP.  
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pH   the inverse logarithm of the H+ concentration; ranges from 0-14. H+ high means low pH(acidic) and H+ low means high pH(basic)  
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3 organs involved in regulation of acid base balance   bones, lungs, kidneys  
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pH of blood   7.35-7.45  
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functions of acids   byproducts of energy metabolism(carbonic acid, lactic acid), digestion(HCl), food for brain(ketoacids)  
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volatile acid   carbonic acid (H2CO3); can be eliminated as CO2  
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nonvolatile acid   lactic acid, sulfuric, phosphoric acids; eliminated through kidneys  
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An increase in CO2 will cause:   increase in CO2, increase in H+, increase in bicarbonate  
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buffer   absorb excessive hydrogen (H+) or hydroxyl (OH-) and prevent significnant change in pH.  
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important buffering systems   carbonic acid- bicarbonate system and hemoglobin  
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carbonic acid bicarbonate buffer system   CO2+H2O<-->H2CO3<-->H+ + HCO3- . The greater the partial pressure of carbon dioxide, the more carbonic acid is formed.  
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respiratory acidosis   increased pCO2, increased carbonic acid, increased H+(low pH), increased bicarbonate. Result of ventilation depression  
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respiratory alkalosis   decreased pCO2, decreased carbonic acid, decreased H+(high pH), decreased bicarbonate. Result of hyperventilation  
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metabolic acidosis   increased levels of ketoacids, lactic acid. Decreased bicarbonate levels, increased H+(low pH)--> heavier breathing causes decreased pCO2  
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metabolic alkalosis   decreased H+ levels, increased bicarbonate levels--> lighter breathing causes increased pCO2  
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compensations   renal and respiratory adjustments to changes in pH . (Production of acidic or alkaline urine, or change in ventilation)  
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protein buffering   proteins have negative charges, so they can serve as buffers for H+  
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renal buffering   secretion of H+ in the urine and reabsorption of HCO3-  
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cellular ion exchange   exchange of K+ for H+ in acidosis and alkalosis  
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anion gap   the difference between the plasma concentration of major cation (Na+) and sum of measured anions (Cl- and HCO3-). Represents concentration of unmeasured anions. Na- (Cl+HCO3-). Normal is 8-12. Increased in lactic acidosis, ketoacidosis  
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Abnormal anion gap (indications)   abnormal anion gap is a result of an increased level of an abnormal unmeasured anion. Examples: diabetic ketoacidosis, lactic acidosis  
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Respiratory System as regulator of acid base balance   eliminates CO2, medulla controls breathing. Increased respirations lead to decreased CO2(hyperventilations).  
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Renal System as a regulator of acid base balance   eliminates H+ and reabsorbs HCO3-. Also reabsorbs/secretes electrolytes. Kidneys decrease/increase urine pH  
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Respiratory Acid base Imbalances   affect carbonic acid concentration (CO2)  
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metabolic acid base imbalances   affect bicarbonate  
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Respiratory Acidosis Causes   hypoventilation(slow breathing gives a carbonic acid/CO2 excess), respiratory failure(raises CO2)  
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Respiratory Acidosis Compensation   kidneys conserve HCO3- and secrete H+ into urine(metabolic alkalosis)  
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Respiratory Alkalosis Causes   hyperventilation(causes deficit in carbonic acid/CO2), hypoxemia from acute pulmonary disorders  
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Respiratory Alkalosis Compensation   rarely occurs due to aggressive treatment of causes of hypoxemia.  
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Metabolic Acidosis Causes   bicarbonate deficit caused by ketoacidosis, lactic acid accumulation, severe diarrhea, kidney disease  
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Metabolic Acidosis Compensation   increased CO2 excretion by lungs (respiratory alkalosis)  
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Metabolic Alkalosis Causes   bicarbonate excess caused by prolonged vomiting and gain of HCO3-  
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Metabolic Alkalosis Compensation   decreased respiratory rate to increase CO2, renal excretion of HCO3-(respiratory acidosis)  
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main sign of dehydration   weight loss (1 L=1 kg=2.2 lbs)  
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Diagnostic criteria for dehydration   a BUN/creatine ratio of >25:1,OR orthostasis, OR a pulse of >100 beats/minute, OR a pulse change of 10-20 beats/minabove baseline with a change in position  
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orthostasis   drop in systolic BP >20 mmHg upon a change of position  
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Hypertonic Dehydration   primarily fluid deficit; more water than salt is being lost  
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Hypotonic Dehydration   primarily sodium deficit; more salt than water is being lost  
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isotonic Dehydration   combined water and sodium deficit; both salt and water are lost proportionately  
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formula for fluid replacement therapy in hypernatremia   calculate free water deficit: .6 x body weight(kg) x [(plasma Na/140) -1] OR Change in serum sodium= (infusate sodium-serum sodium)/(TBW+1)  
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electrolytes lab tests   usually provides info about serum Na, K, Cl, HCO3-  
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BUN and Cr lab tests   indication of renal perfusion; elevated BUN reflects intravascular depletion; Cr indicates acute renal failure  
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CBC lab test   info on hemoconcentration secondary to dehydration; WBCs and differential indicators of infection; platelets can elevate as acute phase reactants  
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UA lab test   specific gravity of urine related to hydration state; in renal disease, can help classify condition; urine ions aid in determining if Na is being retained or not  
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total protein lab test   indirect measures of live function, dietary protein intake, and renal loss.  
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arterial blood gas test   aids in classification of acidosis and alkalosis. Give info on bicarbonate levels  
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Interpretation of ABGs (5 steps)   1) evaluate pH (tells you if its alkalosis or acidosis). 2) Analyze pCO2. 3) Analyze HCO3-. 4) Determine if CO2 or HCO3- matches the pH alteration (respiratory vs. metabolic). 5) Decide if the body is trying to compensate (is pH normal or not?)  
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ROME   Respiratory Opposite= up pH down CO2(alkalosis) and down pH up CO2(acidosis). Metabolic equal= up pH up CO2 (alkalosis) and down pH down CO2(acidosis)  
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partial compensation   after HOURS of acid bas imbalance, the lungs or kidneys will try to bring pH back to normal. ALL parameters will be outside of normal range  
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full compensation   after days or months of untreated acid base imbalance, the pH will be back to normal range, but all other parameters will be abnormal  
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acidemia   more acidic than normal (pH is acidic compared to normal pH of 7.4 but pH still doesnt tell us if it is a respiratory or a metabolic problem)  
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bicarbonate levels as an indicator for acid base imbalance   bicarbonate levels measure metabolic acidosis when a patient has no respiratory abnormality  
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alkalemia   more basic than normal (when the pH rises above 7.45)  
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