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Chpt 2

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
atrophy   decrease, shrinking cell size  
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lipofuscin   yellow-brown age pigment; liver, myocardial, atrophic cells  
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hypertrophy   increase size of cells/organs  
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ANP   atrial natriuretic peptide, early dvlpmnt; cardiac hypertrophy  
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BNP   B-type natriuretic peptide; heart ventricles, Na+, water excretion, vasodilate, inhibit renin  
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hyperplasia   increase number of cells, response to injury growth factor causes mitotic div, DNA synth.  
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compensatory hyperplasia   liver regeneration, ex; 70% regen in 2 wks.  
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hormonal hyperplasia   endometrium-fertilization  
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pathologic hyperplasia   abn proliferation; most common-endometrium with excess bleeding; poss malign transformation  
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Dysplasia   abn change in size, shape, organization of mature cells, NOT ca, may not progress to ca  
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atypical hyperplasia   another name for dysplasia  
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Common site for dysplasia   cervix-results of pap smear; respiratory tract. reversible of stimuli removed  
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metaplasia   reversible replacement of mature cell by another; ex: bronchial from smoking-no cilia  
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Adaptive cellular injury   atrophy, hypertrophy, hyperplasia, metaplasia  
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necrosis   cell death-cell swelling; organelle breakdown  
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apoptosis   cellular self-destruction for elimination of unwanted cell population  
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reversible cell injury   loss of ATP, cell swelling, detach ribosomes, autophagy of lysosomes  
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irreversible cell injury   vacuolization of mitochondria; Ca++ moves into cell; membrane damage (free radicals, enzyme release)  
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Most common cause of cellular injury   hypoxia; most common cause of hypoxia is ischemia  
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repurfusion injury   excess ROS and Ca++ overload to mitochondria can cause cell death (apoptosis)  
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ROS   reactive oxygen species; free radicals: superoxide, hydrogen peroxide, hydroxyl  
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oxidative stress   excess ROS overwhelms endogenous antioxidants, leftover radicals cause cell damage  
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result of ATP depletion   1) Na/K pump decreased, increase cellular Na,Ca; increase extracellular K = cell swelling 2) increase glycolysis=lactate=H+  
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vacuolation   formation of vacuoles, cytoplasmic sm. cavity if oxygen not restored to mitochondria  
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paracetamol   same as acetaminophen outside US  
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Subdural hematoma   blood below dura mater; between dura mater and brain from small vein rupture  
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epidural hematoma   blood above dura mater; between skull and dura; arterial  
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hypercalcemia   hyperparathyroidism, toxic levels of Vit D, hyperthyroidism, Addisons, bone tumor, leukemia  
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necrosis   accidental death, cell swelling, lysis, inflammatory response  
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karyolysis   nuclear dissolution and lysis of chromatin by hydrolytic enzymes-dissolve pyknosis  
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pyknosis   nucleus shrinks and become mass of genetic material  
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Apoptosis   active process of cellular self-distruction; normal or pathologic  
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apoptosis differences from necrosis   scattered, single cells, cell shrinkage & phagocytosis; minimal inflammation  
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manifestation of cell injury   fever, > HR, leukocytosis, pain, cellular enzymes presence  
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pyrogens   cause fever: interleukin-1, tumor necrosi factor-a, prostaglandins  
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CK   creatine kinase; release from muscles, brain & heart  
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troponin   release from heart muscles  
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ALT   alanine aminotransferase (SGPT); release from liver, kidney & heart  
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AST   aspartate aminotransferase (SGOT) ; release from heart, liver, muscles, kidney, pancreas  
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ALP   alkaline phospatase, release from liver, bone  
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amylase   release from pancreas  
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aldolase   release from muscles, heart  
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coagulative necrosis   kidney, heart, adrenal glands; chemical injury (esp mercuric Cl-)protein denaturation-albumin turns to egg white type substance  
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liquefactive necrosis   ischemic brain cells digested by own hydrolases, become liquid filled cyst; Or from neutrophilic hydrolases of bacterial (staph, strep, E.coli)  
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caseous necrosis   tubercolous pulmonary infection, combinaton of coag and liquid necrosis  
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fat necrosis   lipase break down free fatty acids; in breast, pancreas & other abd structures  
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gangrenous necrosis   dry-coagulative; wet-liquefactive from neutrophil  
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gas gangrene   anaerobic bacterial-clostridium-cause bubbles to form in muscle cells; can be fatal if lyse membranes of RBC; death from shock  
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telomeres   end of chromosomes-maintain stability; shorten with aging  
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FOXO   forkhead box O, transcription factor affected by insulin-like signaling  
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Insulin Theory of aging   reduce insulin/IGF-1 by calorie restriction, exercise, wt loss; increase antioxidant enzymes and protein that promote DNA repair  
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DNA theory of aging   DNA damage remodels chromatin (DNA protein)  
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Extracellular changes of aging   increase cross-linking, < collagen, loss of elastin (wrinkles). Vessel deposits-arteriosclerosis  
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Wear and tear theory   small incremental changes as a result of accumulation of small, imperceptible injuries; r/t oxidative stress that damages cells (or malignant DNA damage)  
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Cellular aging   possible from apoptosis initiate cellular adaptations. mitochondria DNA (mDNA) mutations where deletion of protein DNA (heteroplasmy)  
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tissue & systemic aging   stiffness & rigidity tissue changes; > peripheral resistance. thymus atrophy affect endocrine & immune system  
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somatic death   death of the entire person  
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sarcopenia   loss of muscle mass and strength; assoc with fraility  
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somatic death   death of entire person  
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algor mortis   postmortem reduction in body temperature. 1-1.5 degree F/hr. room temp by 24hrs  
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livor mortis   purple discoloration from dependent drainage of blood  
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rigor mortis   muscle stiffening from depletion of ATP begins within 6 hrs, complete by 12-14 hrs, deminishes p next 24-48 hrs.  
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postmorem autolysis   putrefactive changes from release of enzymes and lytic dissolution  
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