Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
154 Cards in this Set
- Front
- Back
hyperplasia
|
increased cell number
|
|
hypertrophy
|
increased cell mass
|
|
atrophy
|
decreased cell mass
|
|
metaplasia
|
change from 1 mature cell type to another
|
|
subcellular alterations in various organelles
|
cell's response to mild chronic injury
|
|
intracellular accumulations, calcifications
|
cell's response to metabolic alterations
|
|
shrinkage
|
apoptotic change in cell size
|
|
fragmentation into nucleosome size fragments
|
apoptotic change in nucleus
|
|
intact; altered structure, especially orientation of lipids
|
apoptotic change in plasma membrane
|
|
no
|
is there adjacent inflammation with apoptosis?
|
|
enlarged, swelling
|
necrotic change in cell size
|
|
pyknosis, karyorrhexis and karyolysis
|
necrotic change in nucleus
|
|
disrupted
|
necrotic change in plasma membrane
|
|
enzymatic digetsion, may leak out of cell
|
necrotic change in cell contents
|
|
intact, may be released in apoptotic bodies
|
apoptotic change in cell contents
|
|
yes
|
does adjacent inflammation occur with necrosis?
|
|
inability to make ATP
|
oxygen deprivation is important to cell injury because:
|
|
hypoxia, physical agents, chemical agents, infectious agents, immunologic reactions, genetic derangement, nutritional imbalances
|
7 causes of cell injury
|
|
aerobic respiration, maintenance of cell membrane integrity, protein synthesis, intracellular cytoskeleton, integrity of genetic apparatus
|
5 essential cellular components to cell injury
|
|
ATP depletion, mitochondrial damage, influx of intracellular Ca, accumulation of ROS, defects in membrane permeability
|
5 general pathways of cell injury
|
|
increased intracellular Ca
|
mechanism of cell injury that activates phospholipases, proteases, ATPases and endonucleases
|
|
mitochondrial damage
|
mechanism of cell injury that leads to leaking of cytochrome c
|
|
ATP depletion
|
mechanism of cell injury that leads to intracellular acidosis and decreased maintenance of ionic gradients
|
|
absorption of radiation, enzymatic metabolism of exogenous chemicals, reduction-oxidation reactions, transition metals, NO
|
5 mechanisms by which free radicals are formed
|
|
anti-oxidants, bound to storage and transport proteins, scavenger enzymes
|
3 mechanisms by which free radicals are made inactive
|
|
scavenge and block initiation
|
what is the manner in which anti-oxidants neutralize free radicals?
|
|
creatine kinase, troponin
|
enzyme markers of cardiac cell death
|
|
transaminases
|
enzyme marker of hepatocyte cell death
|
|
alkaline phosphatase
|
enzyme marker of hepatic bile duct epithelium cell death
|
|
more eosinophilic and fragmented cell membranes
|
2 distinguishing characteristics of necrotic cell
|
|
pyknosis
|
small, dense nucleus
|
|
karyolysis
|
faint, dissolved nucleus
|
|
karyorrhexis
|
fragmented nucleus
|
|
coagulative necrosis
|
alterations in a dead or dying cell, protein degradation and preservation of cell and tissue framework
|
|
coagulative necrosis
|
most common type of necrosis
|
|
liquefactive necrosis
|
occurs when heterolysis or autolysis predominates over protein denaturation
|
|
brain and localized bacterial infections
|
sites where liquefactive necrosis is most often seen
|
|
caseous necrosis
|
necrosis type associated with TB
|
|
lipase activation releasing fatty acids from triglycerides then complexing to Ca to make soaps
|
cause of fat necrosis
|
|
detachment of ribosomes
|
why does hypoxia/ischemia cause decreased protein synthesis?
|
|
ATP depletion
|
what causes change in MPT and pore formation in the mitochondria?
|
|
neutrophil
|
reperfusion injury is associated with what cell type?
|
|
indirectly by transforming to toxic metabolites
|
what type of cell injury to CCl4 and acetaminophen cause?
|
|
caspase activation
|
what is the common outcome of the apoptotic pathways?
|
|
extrinsic (receptor initiated) and intrinsic (mitochondrial)
|
what are the 2 pathways of apoptosis initiation?
|
|
TNF (TNF and Fas)
|
of what receptor family due the death receptor belong?
|
|
Bcl-2 and Bcl-x
|
What are the main 2 anti-apoptotic proteins?
|
|
Bak, Bax, Bim
|
What are some pro-apoptotic proteins?
|
|
caspase 8 and 9
|
What are the initiator caspases?
|
|
caspase 3 and 6
|
What are the executioner caspases?
|
|
intrinsic pathway
|
What pathway of apoptosis is stimulated with growth factor deprivation?
|
|
tumor-suppressor gene p53
|
What accumulates as a result of DNA damage causing the cell to arrest in G1 or go directly into apoptosis?
|
|
Fas
|
What receptor is important in autoimmune diseases and eliminating lymphocytes?
|
|
perforin and granzyme B
|
What substances do cytotoxic T lymphocytes (CTL) secrete upon recognition of foreign agents?
|
|
perforin
|
transmembrane pore-forming molecule
|
|
granzyme B
|
CTL-derived serine protease that cleaves proteins at aspartate residues causing caspase activation
|
|
cancer (hormone-dep, p53 mutations), autoimmune disorder
|
disorders with defective apoptosis and increased cell survival
|
|
neurodegenerative diseases, ischemic injury (MI, stroke), death of virus infected cells
|
disorder with increased apoptosis and increased cell survival
|
|
heterophagy (macrophages action, reabsorption of protein in renal tubules)
|
uptake and degradation of materials from external environment by phagocytosis; name examples
|
|
autophagy
|
lysosomal degradation of degenerating intracellular organelles
|
|
residual bodies (ex lipofuscin, carbon)
|
accumulation of undigested material in a lysosome
|
|
sER
|
intracellular site for metabolizing exogenous agents and typically involves the mixed-function oxidase pathway (P450)
|
|
hypertrophy (induction) of the sER caused by chronic ingestion of certain drugs
|
What causes increased tolerance to certain drugs and an increased capacity to metabolize other drugs?
|
|
Mallory bodies
|
abnormal intracellular accumulation of intermediate filaments
|
|
ER
|
Where does alpha-antitrypsin accumulate with alpha-antitrypsin disease?
|
|
macrophages and mesenchymal cells
|
In what cell types does cholesterol accumulate with xanthoma?
|
|
cholesterolosis
|
focal accumulation of cholesterol-laden macrophages in the lamina of the gallbladder
|
|
Niewmann-Pick disease, type C
|
lysosomal disease due to mutation in enzyme involved in cholesterol catabolism
|
|
excessive synthesis, absorption, abnormal folding or cellular transport defects
|
causes of abnormal protein accumulation
|
|
chaperone
|
name of the protein that stabilizes unfolded proteins to prevent aggregation:
|
|
hyaline
|
any alteration within cells or in the extracellular space that imparts a homogeneous glassy pink appearance in H&E
|
|
intracellular hyaline change
|
proximal tubule epith protein droplets, Russell bodies, viral inclusions and Mallory bodies are examples of:
|
|
extracellular hyaline change
|
occur in damaged arteries due to extravasated proteins:
|
|
glycogenoses and diabetes
|
2 classifications of diseases that cause glycogen accumulation:
|
|
anthracosis
|
deposits are called ____ when they accumulate in pulmonary macrophages and lymph nodes
|
|
hemosiderin
|
hemoglobin-derived golden yellow brown granular intracellular pigment composed of aggregated ferritin
|
|
dystrophic and metastatic
|
2 classifications of calcifications:
|
|
dystrophic calcification
|
occur in nonviable or dying tissues in the presence of normal Ca levels
|
|
metastatic calcification
|
occur in viable tissue and is associated with hypercalcemia
|
|
on membrane-bound vesicles from dead or dying cells that concentrate Ca
|
Where is extracellular calcification initiated?
|
|
mitochondria of dead or dying cells
|
Where does intracellular initiation of calcification occur?
|
|
propagation
|
What step follow initiation in the process of calcification?
|
|
increased PTH, destruction of bone tissue, Vit D-related disorders and renal failure
|
What the 4 classifications of causes of metastatic calcification?
|
|
Paget's disease
|
accelerated bone turnover
|
|
secondary hyperparathyroidism due to phosphate retention
|
How does renal failure cause calcification?
|
|
replicative senescence, genes that influence aging process, progressive accumulation of metabolic and genetic damage
|
3 processes that account for cellular aging:
|
|
telomere shortening
|
incomplete replication of chromosome ends
|
|
IGF-1
|
mutations in this gene can result in prolonged life span:
|
|
dysplasia
|
disordered growth and maturation of the cellular components of a tissue
|
|
superoxide
|
produced by leaks in mitochondrial e- transport chain or in inflam response; type of ROS
|
|
hydrogen peroxide
|
catabolization product of superoxide and SOD and is produced directly by a number of oxidases; type of ROS
|
|
catalase and GPX
|
metabolizes hydrogen peroxide to water
|
|
hypochlorite
|
myeloperoxidase transfers hydrogen peroxide to ____ in neutrophils
|
|
GSH
|
GPX uses this as a cofactor
|
|
hydroxyl radical
|
formed by radiolysis of water
|
|
Fenton reaction
|
reaction of hydrogen peroxide with Fe to form hydroxyl radicals
|
|
Haber-Weiss reaction
|
reaction of superoxide with hydrogen peroxide to form hydroxyl radical
|
|
hydroxyl radical
|
most reactive ROS
|
|
hydroxyl radical
|
radical involved in lipid peroxidation
|
|
peroxynitrite
|
formed by the interaction of superoxide and nitric oxide
|
|
nitric oxide
|
potent vasodilator and mediator of important biological processes
|
|
SOD
|
first line of defense against superoxide, converts it to hydrogen peroxide and O2
|
|
catalase
|
located in peroxisomes, eliminates hydrogen peroxide to form water and O2
|
|
GPX
|
catalyzes the reduction of hydrogen peroxide and lipid peroxides to water and GSSG
|
|
Vit E (alpha-tocopherol)
|
terminal e- acceptor, exerts activity in lipid membranes
|
|
Vit C (ascorbate)
|
reacts with O2, hydroxyl radical and products of lipid peroxidation, regenerates Vit E
|
|
retinoids
|
precursors of Vit A, chain break antioxidant
|
|
nitric oxide
|
chelates iron, scavenges free radicals, reacts with free radicals to cause damage, increases proteasomal activity, decreases cell uptake of transferrin receptor
|
|
chaperonopathies
|
retinitis pigmentosa, hereditary spastic paraplegia, Hippel-Lindau disease are examples of what grouping of disease?
|
|
channelopathies
|
cardiac arrhythmias, neuromuscular syndromes (myotonias), pediatric epilepsies are examples of what grouping of diseases?
|
|
Lewy bodies (alpha-synuclein)
|
seen in neurons of the substantia nigra of Parkinson disease
|
|
neurofibrillary tangles (tau protein)
|
characterize cortical neurons in Alzheimer disease
|
|
fibrinoid necrosis
|
alteration of injured BVs in which insudation and accumulation of plasma proteins cause the wall to stain intensely with eosin
|
|
Guilford progeria
|
entire process of aging is compressed into span of less than 10 years
|
|
progerin
|
name of the defective protein found in the disease progeria
|
|
Werner syndrome
|
autosomal recessive disease characterized by early cataracts, hair loss, atrophy of skin, osteoporosis and atherosclerosis
|
|
germ cells
|
These cells have the highest telomerase activity:
|
|
apoptosis
|
endometrial breakdown relating to the menstrual cycle is what type of process?
|
|
atrophy
|
Lipofuscin accumulation is a result of what process?
|
|
Ubiquitination
|
What conjugation process often precedes proteosomal degradation of proteins?
|
|
First, Ubiquitin activation, then Ubiquitin conjugation, finally, Ubiquitin ligation.
|
What are steps in the enzymatic cascade of ubiquitination?
|
|
The 26 S proteasome
|
Which type of proteasomes recognizes and degrades ubiquitinated proteins?
|
|
Lysosomes
|
By which cellular organelle is chaperone mediated autophagy (CMA) executed?
|
|
Reduced functional demand
|
What mechanism most often leads to cellular atrophy?
|
|
Activation of ubiquitination
|
How does disuse atrophy cause protein degradation?
|
|
An increase in cell size and functional capacity
|
How is cellular hypertrophy defined?
|
|
Increased protein translation and decreased protein degradation.
|
How can protein production increase in the absence of increased transrciption?
|
|
Activation of signaling to inhibit apoptosis
|
How does the process of hypertrophy affect cell survival?
|
|
Increased functional demand
|
Moving from sea level to high altitude results in increased red blood cell mass. What mechanism of hyperplasia does this illustrate?
|
|
Conversion of one differentiated cell type to another
|
Define Metaplasia?
|
|
Glandular Metaplasia called Barrett’s esophagus
|
Chronic gastro-esophageal reflux leads to what type of of metaplastic change in the esophagus?
|
|
Dysplasia
|
If histologic examination shows disordered cellular maturation and growth, what diagnosis applies?
|
|
Dystrophic calcification
|
What is the term for mineral deposition in an area of necrosis?
|
|
Hydropic Swelling
|
How do we describe and increase of cellular volume due to increased water content?
|
|
Sodium Potassium ATP-ase, located at the cell membrane
|
What enzyme constitutes the sodium potassium pump and where is it located?
|
|
By cytochrome oxidase
|
How is molecular oxygen reduced to water in the cell?
|
|
Superoxide, peroxide, and the hydroxyl radical
|
What are the intermediate species in the reduction of molecular oxygen to water?
|
|
By catalase and glutathione peroxidase (GPX)
|
How does the cell detoxify peroxide?
|
|
It may both protect from injury and augment injury caused by reactive oxygen species
|
How does nitric oxide affect cellular damage by reactive oxygen species?
|
|
Chaperonopathies
|
What is the term for the disease of proteins that guide other proteins to fold correctly?
|
|
In adipocyte’s fat
|
Where and in what form is most of the body’s excess energy stored?
|
|
Xanthoma
|
When clusters of cholesterol laden macrophages accumulate in subcutaneous tissues, what is the structure that they form?
|
|
Prions
|
Protein particles that lead to protein misfolding belong to what class of transmissible agents?
|
|
They are oxidized which alter’s proteins tertiary structure
|
How are proteins affected in age related impairment of axtioxidant defenses?
|
|
By forming aggregates
|
How do misfolded proteins escape degradation in severe oxidative stress?
|
|
Lipofusion inhibits both lysosomal and proteasomal protein degradation
|
How does lipofusion affect protein processing?
|
|
Oxidative stress
|
What is the mechanism of tissue damage in ischemia reperfusion injury?
|
|
Hemosiderosis
|
What is the term for increased iron storage in the body?
|
|
Transforming growth factor alpha
|
Which cytokine is responsible for increased neutrophil chemotaxis at sites of ischemia or reperfusion injury?
|
|
Trauma and pancreatitis
|
What are the most common causes of fat necrosis?
|
|
Calcium activates phospholipase A 2, which degrades membrane phospholipids
|
How does intracellular calcium accumulation in hypoxic injury affect cell membrane integrity?
|
|
Procaspase 8 is activated to caspase 8
|
Which enzyme is activated by granzyme B and what is its activated derivative?
|
|
Cell survival
|
If the mitochondrial membrane contains a proponderance of homodimers of BCL 2, what would the expected result be?
|
|
P53
|
What is the binding target of MDM 2?
|