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McCance Patho Wk 1
Chpt 2
| Question | Answer |
|---|---|
| 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 |
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