Chpt 2
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
---|---|---|---|---|---|
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
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Created by:
Tabble
Popular Physiology sets