Reading...
Play button
Play button
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;
127 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is pathogenesis and what does it dictate?
|
mechanisms of the disease development which dictate the symptoms of the disease
|
|
|
|
How can a disease by classified?
|
Etiology, Pathogenetic mechanisms, Organ system
|
|
|
|
What are the 6 most common causes of death?
|
Heart, Cancer, Stroke, Obstructive lung disease, Trauma, Diabetes.
|
Hef Can Stroke OLD Tiny Dick
|
|
|
What are frozen sections?
|
Parts removed by surgeon to determine margins of resection, etc, while patient is under anesthesia
|
|
|
|
What is the evaluation of cells removed from organ or fluid?
|
cytopathology
|
|
|
|
What does hormone-induced breast enlargement an example of?
|
hyperplasia (number of cells increase)
|
also regeneration of liver; these are physiologic hyperplasias
|
|
|
What is hyperplasia dependent upon?
|
growth factors, hormone, and cytokines
|
|
|
|
What may endometrial hyperplasia result from?
|
excessive estrogen or unopposed estrogen
|
This is an example of pathologic hyperplasia
|
|
|
Hyperplastic tissues have an increased chance of what?
|
developing cancer
|
|
|
|
What causes hypertrophy?
|
increased workload
|
|
|
|
What does hemodynamic overload in cardiac muscle cause?
|
Cardiac muscle hypertrophy
|
|
|
|
What is re-introduction of ANP in ventricle an example of?
|
hypertrophy accompanied by changes in gene expression
|
because the body doesn't want to work as much, they get rid of some blood volume with ANP
|
|
|
What may occur secondarily to hypertrophy to allow the body to adjust to the increased workload?
|
gene expression to switch proteins or expression of receptors
|
|
|
|
What causes atrophy?
|
loss of nutrients/innervation/trauma or due to lack of simulatory factors as in developmental atrophy
|
|
|
|
What causes metaplasia?
|
cellular response to an adverse environment
|
|
|
|
What is bone formation in muscle an example of?
|
Myositis ossificans is an example of metaplasia
|
|
|
|
How does metaplasia occur?
|
reprogramming of stem cells or mesenchymal cells
|
|
|
|
What are the mechanisms of cell injury?
|
Ca2+, Oxidative stress, ATP depletion, Loss of membrane function (COAL)
|
|
|
|
How does reversible injury present microscopically?
|
minor changes: swelling and fat vacuoles
|
|
|
|
What is a bleb?
|
an irregular bulge in the plasma membrane of a cell caused by localized decoupling of the cytoskeleton from the plasma membrane; seen in reversible cell injury
|
|
|
|
What are the different types of necrosis?
|
coagulative (basic cell outline preserved), liquefactive, caseous (like cheese), and fat necrosis
|
|
|
|
Reversible or irreversible cell injury: inactivation of Na-K ATPas pump
|
Reversible
|
|
|
|
Reversible or irreversible cell injury: ER swelling due to electrolyte imbalance
|
Reversible
|
|
|
|
Reversible or irreversible cell injury: depletion of glycogen stores and decreased pH
|
Reversible
|
|
|
|
Reversible or irreversible cell injury: Loss of microvilli
|
reversible, alongside blebbing
|
|
|
|
Reversible or irreversible cell injury: Detachment of ribosomes from rough ER
|
reversible
|
|
|
|
Reversible or irreversible cell injury: Loss of mitochondrial membrane function
|
irreversible
|
|
|
|
Reversible or irreversible cell injury: release of acid hydrolases
|
irreversible
|
|
|
|
What is reperfusion injury and who is involved?
|
increased oxygen free radicals in the re-introduction of blood which further cause oxidative damage via cytokine and adhesion molecule recruitment of inflammatory cells
|
|
|
|
What are the three nuclear changes seen in irreversible cell injury?
|
pyknosis(shrunken.dark nucleus, karolysis (chromosome lyase) , karyorrhexis, dark dense fragment chromosomes.
|
|
|
|
How does carbon tetrachloride cause chemical injury to cells?
|
Conversion to CCl3 by P450
|
same with acetaminophen which depletes glutathione
|
|
|
What toxin poisons cytochrome oxidase to cause cellular chemical injury?
|
Cyanide
|
|
|
|
How do free radicals cause cellular damage?
|
peroxidation of membranes, cross-linking and oxidation of AA, breaking DNA
|
|
|
|
What control free radicals?
|
Vitamins A and E, sequestration of metals by transferrin and ceruloplasmin, enzyme degradation (catalase, glutathione, superoxide dismutase)
|
|
|
|
What are the causes of apoptosis?
|
embryogenesis, homeostasis, aging
|
|
|
|
What are the morphologic changes that accompany apoptosis?
|
Cell shrink, chromatin condense, cytoplasmic blebs
|
|
|
|
What process includes phagocytosis without inflammation?
|
apoptosis
|
|
|
|
What biochemical changes are involved with apoptosis?
|
protein cleavage by capsases, DNA breakdown, phagocytic recognition
|
|
|
|
What two models are implicated in apoptotic signalling pathways?
|
TNF and Fas transduction
|
due to loss of GF or hormones
|
|
|
What is released by mitochrondria during apoptosis?
|
cytochrome C
|
|
|
|
What proteins control apoptotic mechanisms?
|
p53 and Bcl-2 proteins
|
|
|
|
What processes respond to cell injury
|
lysosome catabolism, ER hypertrophy, mitochondrial changes, cytoskeletal changes
|
|
|
|
What type of subcellular change: alcoholic liver disease.
|
mitochondrial
|
|
|
|
What type of subcellular change: nutritional deficiency
|
mitochondrial
|
|
|
|
What type of subcellular change: oncocytoma
|
mitochondrial
|
|
|
|
What type of subcellular change: tattoos and anthracosis
|
lysosome catabolism
|
|
|
|
What type of subcellular change: increased workload of P450
|
smoothER hypertrophy
|
|
|
|
What type of subcellular change: kartagener syndrome
|
cytoskeletal
|
|
|
|
What type of subcellular change: colchicine
|
cytoskeletal
|
|
|
|
What type of subcellular change: phalloidin
|
cytoskeletal
|
toxin
|
|
|
What is mallory hyaline?
|
aka Mallory body, it is an inclusion in cytoplasm of liver cells seen in alcoholics
|
has a eosinophilic, twisted rope appearance
|
|
|
What is a hyaline change?
|
a smooth glassy, pink appearance due to accumulation of a proteinaceous material (cytoskeleton, Ig's)
|
|
|
|
What is steatosis stainable with?
|
Sudan IV or Oil Red O
|
|
|
|
What intracellular accumulation is seen in steatosis?
|
triglycerides in droplets
|
|
|
|
What intracellular accumulation is seen in atherosclerotic plaques
|
foam cells in intima
|
|
|
|
What intracellular accumulation is seen in xanthomas
|
cholesterol in macrophages in soft tissues and tendons
|
|
|
|
What is a russell body?
|
Ig accumulations in plasma cells
|
|
|
|
What can bee seen in renal tubular cells in proteinuria?
|
reabsorption droplets of protein
|
|
|
|
What color are amyloids in polarized light with the congo red stain?
|
apple green
|
|
|
|
Where can glycogen accumulate in diabetes?
|
renal tubular cells, hepatocytes, islet cells
|
|
|
|
What is Pompe's?
|
a glycogen storage disease
|
|
|
|
What is seen in anthracosis?
|
carbon deposists in lung and lymph nodes
|
black lung disease
|
|
|
What is tattooing?
|
Pigment phagocytized by dermal macrophages
|
|
|
|
What is lipofusin?
|
oxidized lipids in lysosomes in heart and liver
|
fat soluble pigment that is the end product of membrane lipid peroxidation
|
|
|
What can be detected by viewing tissue under prussian blue stain?
|
hemosiderin
|
hemosiderosis is the pathological process, hemochromatosis is the disease state.
|
|
|
What may be seen in papillary cancers
|
Lamellated psammoma bodies
|
sammoma = sand; these are pearl-like calcifications
|
|
|
What are the theories of cellular aging?
|
telomere shortening, clock genes AND accumulated damage.
|
|
|
|
What syndrome is characterized by percocious aging?
|
Werner's syndrome
|
AR and occurs at puberty due to shorter telomeres
|
|
|
What are the differences in electrophoretic analysis between necrosis and apoptosis?
|
DNA fragmentation is random in necrosis where as apoptosis are fragmented at endosomal boundaries and result in a ladder dna pattern
|
|
|
|
What are the two components of the inflammatory response?
|
vascular reaction and a cellular reaction, both of which are mediated by chemical factors.
|
|
|
|
What cells mediate an acute inflammatory response?
|
Neutrophils,
|
|
|
|
What cells mediate a chronic inflammatory response?
|
macrophages, lymphocytes, eosinophils, plasma cells and mast cells.
|
|
|
|
What inflammatory reponse would be characterized by neovascularization, tissue necrosis, and fibrosis?
|
chronic inflammation
|
|
|
|
What are some de novo causes of chronic inflammation?
|
TB, syphilis, leprosy, silicosis, arthritis, lupus
|
|
|
|
What are the cardinal signs of inflammation?
|
Rubor, tumor, calor, dolor, functio laesa
|
|
|
|
After the acceptance of the cardinal signs of inflammation, what other observations were made?
|
it occurs in living tissue, phagocytosis, humoral immunity, chemical mediators
|
|
|
|
What are the chemical mediators of inflammation?
|
Histamine, Serotonin, Complement, Kinin, Clotting factors.
|
|
|
|
What do the following indicate: vlisters, inflammation of linings of cavities, pus, and ulcers.
|
Acute inflammation morphologic patters
|
|
|
|
What is a granuloma?
|
an accumulation of activated macrophages
|
|
|
|
What causes caseating granulomas?
|
tuberculosos
|
|
|
|
What causes non-caseating granulomas
|
sarcoidosis
|
|
|
|
What are the systemic effects of inflammation?
|
fever, sepsis, leukocytosis, acute-phase reactions, other.
|
|
|
|
What are the acute-phase reactants?
|
C-reactive protein, fibrinogen, serum amyloid A
|
|
|
|
What is the leukemoid reactoin?
|
Left shift of leukocytes that looks like leukemia but is just increase in immature cells.
|
|
|
|
What is the difference between regeneration and healing?
|
regeneration requires intact ECM, labile or stabile cells, and leaves no scar.
Healing involves inflammatory processes and cell necrosis in organs incapable of regeneration |
|
|
|
What is a scar?
|
healing of a wound where the ECM framework is damaged and tissue architecture is altered
|
|
|
|
What are the labile tissues?
|
bone marrow, epithelium, and stem cells
|
|
|
|
What are the stabile tissues?
|
kidney/liver/pancrease parenchyma, endothelium, fibroblasts, osteo/chondrocytes, SMOOTH MUSCLE
|
tissues that have low replication but can replicate rapidly in response to stimuli
|
|
|
What are permanent tissues unable to undergo mitotic division in postnatal life?
|
neurons, skeletal muscle, cardiac muscle
|
|
|
|
What occurs when neurons, skeletal muscle, or cardiac muscle become injured?
|
they are replaced by scar tissue
|
these are permanent tissues unable to undergo mitosis
|
|
|
What do stem cells in the following develop into: Liver
|
Liver stem cells (in canal of Hering) --> oval --> hepatocyte or biliary cells
|
|
|
|
What do stem cells in the following develop into: Brain
|
unknown importance
|
|
|
|
What do stem cells in the following develop into: skeletal muscle
|
satellite cells (myocytic, osteogenic, adipogenic)
|
|
|
|
What do stem cells in the following develop into: epithelial tissue
|
stem cell --> intermediate cells --> differentiated cells
|
|
|
|
What determines reconstitution of cells after injury?
|
1) increased growth fraction
2) increased number of replications 3) increased rate of mitosis |
|
|
|
What are EGF and TGF produced by?
|
keratinocytes, macrophages, inflammatory cells
|
|
|
|
What dpes upregulation of the ERB B2 and HER-2/neu receptors result in?
|
breast cancer
|
these are EGF receptors
|
|
|
What is scatter factor?
|
HGF; induces cells to form one layer and away from each other into open space
|
|
|
|
What does platelet derived growth factor stimulate?
|
causes migration and proliferation of fibroblasts, smooth muscle cells, and monocytes
|
ties inflammation, clotting cascade, and healing
|
|
|
What cemical mediator dies together the inflammatory response, clotting cascade, and healing?
|
Platelet-derived growth factor which causes migration and proliferation of fibroblasts, smooth muscle and monocytes; released upon platelet activation
|
|
|
|
What binds to heparan sulfate in ECM and promotes synthesis of extracellular matrix protein?
|
fibroblast growth factor
|
|
|
|
What induces myoblast proliferation, lung maturation, and hepatocyte differentiation?
|
fibroblast growth factor
|
|
|
|
What does transforming growth factor do?
|
STIMULATES SCAR TISSUE; fibrogenic agent and inhibits epithelium and leukocytes.
|
|
|
|
What does liver regeneration accomplish?
|
recovery of mass, not form (hepatocytes and nonparenchymal cells such as blood vessels, biliary ducts)
|
|
|
|
What are the three steps of liver regeneration?
|
Priming, proliferation, and cgrowth cessation
|
|
|
|
What mediators are responsible for Go-Gi transition during liver regeneration?
|
TNF and IL-6
|
priming stage of liver regeneration
|
|
|
What mediators are responsible for proliferation of hepatocytes?
|
HGF and TGF-a
|
|
|
|
What mediators are responsible for cessation of liver regeneration?
|
TGF-B
|
|
|
|
What defect is seen in patients with marfan syndrome?
|
defects in elastic fibers
|
|
|
|
What do cadherins mediate?
|
cell to cell interaction w desmosomes and zonula adherens
|
|
|
|
What do osteonectins regulate?
|
tissue remodeling and angiogenesis inhibition
|
|
|
|
What does thrombospondin do?
|
inhibit angiogenesis
|
|
|
|
What does Osteopontin do?
|
regulates calcification and mediates leukocyte migration
|
|
|
|
What does tenacin do?
|
morphogenesis and cell adhesion
|
|
|
|
What inhibits cell to cell adhesion and facilitates cell motility?
|
hyaluronic acid
|
|
|
|
What cells does angiogenesis stem from?
|
angioblasts from hematopoietic precursors stored in bone marrow
|
|
|
|
What chemical mediators are involved with angiogenesis?
|
VEGF, Angiopoeitins, PDGF and TGF-B
|
|
|
|
What causes scar formation?
|
fibroblast deposition of collagen 3-5 days post injury.
|
|
|
|
Why should one cut along lines of stress?
|
tissue remodels along line of force
|
|
|
|
What are the three phases of cutaneous wound healing?
|
inflammation, granulation tissue formation, wound contraction
|
|
|
|
What are the steps of cutaneous wound healing?
|
clogging, neutrophils, macrophages, neovascularization, collagen bridge, regression, scar. (approx 1 mo)
|
CNMNCRS
|
|
|
What is healing by secondary intention?
|
When extensive damage leaves a tissue defect and a more intense inflammatory response is ounted to remove necrotic material
|
|
|
|
Why does fibrosis occur?
|
persistence of initial stimulus or development of chronic immune reaction
|
|
|
|
What is pneumoconiosis?
|
fibrosis of the lung due to coal, asbestos, silica inhalation
|
|
|
|
What is karyolysis?
|
the complete dissolution of the chromatin matter of a dying cell due to the activity of DNAase.
|
|
|
|
What is pyknosis?
|
is the irreversible condensation of chromatin in the nucleus of a cell undergoing apoptosis
|
|
|
|
What is karyorrhexis?
|
fragmentation of the nucleus of a dying cell whereby its chromatin is distributed irregularly throughout the cytoplasm
|
|
