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McCance Patho Wk 1

Chpt 2

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



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