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;
70 Cards in this Set
- Front
- Back
|
cell components may be subject to changes with aging
|
mitochondria, ribosome, membrane, DNA
|
|
|
health state of a cell influences its ability to...
|
resist microorganisms
recover from injury / inflammation |
|
|
aging & wound healing
|
correlation between aging & impairment of wound healing
|
|
|
free radical theory
|
wide presence of free rads induces DNA damage & oxidative stress
|
|
|
telomere aging clock theory
|
molecular mechanisms lead to senscence
acts as anticancer mechanism |
|
|
pathologic changes & aging
|
vary individually
mainly decr fxl reserve d/t atrophy of tissue / organs decr resistance to infection |
|
|
cellular implications of aerobic training
|
improved aerobic capacity
mitochondria improve fx modify damage by reactive O species combines to allow body to reestablish cellular norms |
|
|
chain of cell injury
|
more severe = more lethal to cells
body begins inflammation to remove injurious agent, cellular debris, begin healing regneration of tissue |
|
|
7 mechanisms of cell injury
|
ischemia
infection immune rx genetic factors nutrition physical factors chemical factors |
|
|
reversibility of injury depends on...
|
cell's ability to regain homeostasis
|
|
|
ischemia
|
d/t
reduced blood flow incr metabolic demand results in hypoxia, anoxia, decr nutrients, incr wastes, decr aerobic metabolism occurs most often to decr arterial lumen |
|
|
infectious agents
|
fbacterial: release of exo- & endo- toxins, may induce inflammatory / immune response
viruses: hijack cell for viral replication, disruption of cell membrane with virus-coded proteins embedding into membrane |
|
|
immune reactions
|
hypersensitivities: allergy, anaphylactic rx, autoimmune disorder
allergic rx can range in severity from mild, to severe hypoxia, or anaphylactic shock |
|
|
genetic factors
|
changes in # or structure of chromosomes
single mutations that alter # or fx of proteins multiple mutations interact w/ environment yielding multifactorial disorders |
|
|
nutrition
|
deficiencies of essential amino acids impacts protein synth
vitamin deficiency syndromes, like C & rickets may be d/t factors not associated with food intake |
|
|
physical factors
|
trauma & physical agents can cause cell death directly and may indirectly lead to cell death
temperature, rads, electricity may damage cells |
|
|
mechanical factors
|
tissue fails if applied load > failure tolerance d/t any combo of rate, compression, force type(s)
may result from repetitive tasks or single high-load tasks |
|
|
2 types of chemical factors
|
direct injury
heavy metals disrupt membrane proteins, alkylating agents target body's cells to stop cancer, overdose indirect injury must be metabolically transformed into toxin |
|
|
free radical formation
|
free rads are necessary but can have bad effects
O activated by gain / loss of e⁻ |
|
|
oxygen radicals
|
toxic to cells
result from cellular metabolism O₂⁻, H₂O₂, ⁻OH |
|
|
antioxidants
|
neutralize excess free rads
may be endo- or exo- genous |
|
|
nitric oxide
|
NO
free rad, highly reactive reduced availability linked to many disorders |
|
|
exercise & free rads
|
impact dependent on induced oxidative stress
|
|
|
psychosocial factors & tissue adaptation
|
fear, tension, anxiety may limit healing
|
|
|
reversible injury
|
transient impairment of cell's structure / function
acute: affects ion homeostasis leading to fluid shifts cell has to switch to anaerobic lactic acid accumulates, acidity results slows healing swelling d/t injured Na-K pump leading to altered permeability excess ions in cytoplasm, mitochondria, & ER lead to ∆ in fx |
|
|
characteristics of cellular adaptation
|
change in size, #, fx that incr cell's ability to live
most common types atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia |
|
|
-trophy v -plasia
|
change in # & size v change in number only
|
|
|
intracellular accumulations
|
incr in storage of lipids, proteins, carbs, pigments d/t overload of metabolites / exogenous material
|
|
|
irreversible cell injury
|
positively correlated with extent of magnitude, duration, inability of cell to adapt
|
|
|
lethally injured cells exhibit
|
alterations in nucleus, mitochondria, lysosomes, cell membrane
|
|
|
pyknosis
|
degeneration of cell as nucleus shrinks & chromatin condenses
karyorrhexis: fragmentation of such a cell karyolysis: lysing of such a cell |
|
|
coagulative necrosis
|
d/t ischemia
in solid internal organs or as dry gangrene membrane preserved, pyknosis & karolysis, organelles dissolve |
|
|
caseous necrosis
|
d/t Mycobacterium tuberculosis & other fungal infections
in lungs, bronchopulmonary lymph nodes, skeletal bone cell membrane destroyed, debris is cheese-like, persists indefinitely damaged area walled off in granuloma |
|
|
liquefactive necrosis
|
pyogenic bacteria
in brain tissue, skin, wound, joint infection, as wet gangrene neuron death releases lysosomes that liquefy area, forming abscesses that are shapeless |
|
|
fatty necrosis
|
d/t acute pancreatitis, abdominal trauma
in abdominal area Ca soaps formed by release of pancreatic lipases |
|
|
fibrinoid
|
d/t blood vessel wall trauma
in tunica media & smooth muscle cells plasma proteins accumulate, debris & serum proteins form pink deposits |
|
|
pathologic tissue calcification
|
deposition of Ca salts in body tissues
dystrophic: calcification in damaged tissue metatstatic: occurs w/ hypercalcemia |
|
|
multiple cell injury
|
initial injury can lead to subsequent cell damage due to complications
|
|
|
TBI
|
traumatic brain injury
|
|
|
types of brain damage
|
coup
at site where brain impacts skull countrecoup opposite impact polar at tips of frontal, temporal, occipital lobes & underside of frontal & temporal DAI: diffuse axonal injury subcortical white matter, may involve brain stem secondary d/t HII - hypoxicischemic injury d/t cerebral edema |
|
|
tissue healing
|
regrowth or repair
|
|
|
fibronectin
|
forms scaffold, provides tensile strength, glues other substances & cells together
earliest in healing process |
|
|
proteoglycans & elastin
|
proteoglycans
secr by fibroblasts, bind to fibronectin & collagen to aid tissue stability elastin fibroblasts secr proteins that cross link into fibrils or long sheets |
|
|
collagen
|
most important protein providing structural support & tensile strength
triple helix of amino acids many types, each with specialized functions tendon strength: unidirectional & parallel bundles flexibility of skin, rigidity of bone: random arrangement tensile strength: assembled into thicker & stronger filamentous structures |
|
|
collagen types
|
I: predominates
II: predominates in hyaline cartilage III: in vascular & visceral structures IV: basement membranes, mesenchymal cells, glomeruli V: most tissues, never a major component VI: most connective tissues VII: involved in matrix & bone disorders, anchor lymphatic vessels at dermal/epidermal junction VIII: basement membranes, bridges between matrix molecules IX: minor component of hyaline, vitreous humor X: only in epiphyseal cartilage XI: hyaline XII: embryonic skin & ligament, periodontal ligament XIII: endothelial XIV: fetal skin & tendons XV_XXVII: not understood |
|
|
collagen & PT's
|
unknown efficacy
myofascial techniques, soft tissue mobilization techniques ultrasound incr collagen extensibility, enzymatic activity, absorb joint adhesions, reduce fibrous volume & scar density |
|
|
growth factors
|
reg cell proliferation, differentiation, migration, biosynth, protein degradation, angiogenesis
bind to specific cell receptors to stim or inhibit |
|
|
nutrition
|
healing increases protein catabolism systemically
C deficiency & defective collagen zinc deficiency & decr degradation of collagen & protein synth |
|
|
other factors that influence tissue healing
|
vascular supply
decr nutrient delivery & waste removal, COPD decr SpO₂ Meds corticosteroids, chemo, rads Infection incr length & severity of inflammatory rx which may damage tissues SNS stim (e.g. combat soldiers, abused kid) |
|
|
PT & healing
|
id & mod behaviors that contribute to stressing injured tissues
screen for behaviors that might impact healing training to incr ability to handle stress |
|
|
healing phases
|
hemostasis & degeneration
inflammation proliferation & migration these overlap, rather than being sequential inflammation present from the start proliferation w/in 24 h remodeling & maturation |
|
|
hemostasis & degeneration
|
hemostasis
stop the bleeding degeneration hematoma, necrosis of dead cells |
|
|
inflammation
|
coordinated rx of tissues to cell injury / death involving vascular, humoral, neurologic, & cellular responses
begins once clot forms vasodilation & incr capillary permeability activate movement of various cells these cells destroy invaders, clean up debris, release protease (elastase, collagenase), secrete add'l growth factors |
|
|
acute inflammation
|
follows tissue insult
signs & symptoms redness, swelling, incr temp, pain, decr fx of site |
|
|
chronic inflammation
|
develops if extensive necrosis, can't regenerate parenchymal cells, persistence of underlying cause
hallmarks accumulation of macrophages, lymphocytes, plasma cells granulation tissue comprised of proliferating endothelial cells & fibroblasts granuloma |
|
|
4 cardinal signs/symptoms of inflammation
|
erythema d/t vasodilation
heat d/t vasodilation edema d/t leakage of fluid & cells into extravascular spaces pain direct trauma, bradykinin mediation, histamines, serotonin, internal pressure d/t edema, swelling of nerve ends |
|
|
granuloma
|
< 2mm diam aggregate of macrophages often surrounded by lymphocytes
may flatten as epithelium, may fuse together typical of TB |
|
|
vascular alterations
|
vessel integrity disrupted
flow in surrounding tissue compresses damaged vessels, promotes platelet aggregation if tissue damaged but vessels are intact, arterioles are temporarily constricted via neural input, then vasodilation override |
|
|
transudation
|
leakage of protein-poor fluid from vasculature to interstitial space
|
|
|
leukocyte accumulation
|
margination during stasis
WBC's accumulate & adhere to endothelial cells of vessel walls initiates circulation of WBC from normal areas to inflammation site WBC's then actively migrate out |
|
|
inflammatory exudate: sanguineous
|
bright red, bloody
small amts d/t trauma larger may be hemorrhage sudden & large may be draining hematoma |
|
|
inflammatory exudate: serosanguineous
|
yellow or pink
48-72 h after trauma sudden incr may indicate wound dehiscence |
|
|
inflammatory exudate: serous
|
thin, clear, yellow w/ albumin & immunoglobins
occurs in early stages of most inflammation blisters, joint effusion w/ RA, viral infections sudden incr may indicate draining seroma |
|
|
inflammatory exudate: purulent
|
viscous, cloudy, puss, cell debris from necrotic cells, dying neutrophils
usually d/t purulent bacteria indicates infection sudden incr may be draining boil |
|
|
inflammatory exudate: catarrhal
|
thin, clear mucus
w/ inflammatory processes in mucous membranes |
|
|
inflammatory exudate: fibrinous
|
thin, clear, yellow, pink, tinged, cloudy
w/ severe inflammation or bacterial infections tough to resolve can cause fibrous scarring & restriction |
|
|
cell derived inflammation mediators
|
circulating platelets
tissue mast cells basophils neutrophils endothelial cells monocytes/macrophages injured tissue arachidonic acid derivatives cytokines |
|
|
plasma cell-derived inflammation mediators
|
blood coagulation cascade
fibrinolytic system kinin enzymatic system complement system |
|
|
MI
|
lecture
|
|
|
221
|
221
|
