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46 Cards in this Set
- Front
- Back
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What is the general purpose of adaptation, changes in cell structure and f'n as a result of negative or normal stimulus? |
to try and maintain homeostasis, aka healthy conditions |
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What are the main types of adaptation we talked about |
Atrophy Hypertrophy hyperplasia dysplasia metaplasia |
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atrophy |
When cells get smaller, physiological: when thymus shrinks in children pathologic: too much bed rest, skeletal and cardiac muscles atrophy |
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hypertrophy |
when cells get larger physiologic: body builder pathologic: heart and kidneys (cells that don't do a lot of mitotic division) get larger due to increased difficulty in meeting workload |
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hyperplasia |
when cells increase in # physiologic: removal of liver, it regenerates, or estrogen stimulating endometrium to grow pathologic: imbalance betw estrogen and progesterone secretion, endometriosis |
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dysplasia |
not a true adaptive process, cells just screwed up. abnormal changes in shape, size, organization in mature cells. aka atypical hyperplasia. adjacent to cancer cells. epithelial tissue of respiratory tract in smokers. |
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metaplasia |
reversibile displacement of one cell type with another. pathologic: ciliated pseudostrat go to squamous epithelial cells in the trachea of smokers. physiological: not mentioned. |
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3 sources of INTRAcellular accumulations |
this is result of injury. normal cellular substances:excess water, proteins, lipids, carbs, bilirubin abnormal endogenous: product of abnormal metabolism not effectively catabolized abnormal exogenous: infectios agent, chemical, or mineral |
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oxygen deprivation |
1.atp synth ceases, anaerobic metabol ceases, lactic acid build up 2. Na/K+ pumps shut down, 3. Na comes in, K goes out, Ca comes in 4. water follows Na, swelling 5. ribosomes detach 6. vacuolization 7. influx of Ca activates many enzyme systems: membrane damage, etc. cell death, apoptosis
most common cause of cellular injury |
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physical chemical agents |
toxic chemicals, drugs, CO, pass through lipid membrane, interact directly with proteins/DNA, liver damage also temperature, electrical , radiation |
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infectious agents |
endo and exo toxins, hijacking cellular function, destroys immune rxns |
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immunologic rxns |
anaphylactic rxns. too much of body's own defense , like histamine, massive vasodilation |
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genetic changes |
down syndrome, sickle cell anemia |
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nutritional imbalance |
scurvy (vit c) , beriberi (protein?) |
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mitochondrial damage |
liberates Ca+ in cytosol |
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free radicals |
chain rxn. membrane damage and increased permeability, protein alterations, DNA fragmentation, mitochondrial damage (causing release of Ca+ in cytosol) |
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reversible vs. irreversible cellular injury |
reversible : stimulus goes away, cell can recover. irreversible : death. either programmed with appropriate cell removal or necrosis. |
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4 major types of necrosis type of tissue affected by each |
coagulative: most common. related to ischemia. a lot of protein. kidneys and heart. liquefactive: in tissues w high level of lipids, brain. ischemic injury to neurons and glial cells. fat: breakdown of fat by lipase. pancreas, breast. caseous: TB in lungs. combo of coagulative and liquefactive. |
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difference betw dry and wet gangrene |
dry: arterial problems. skin gets dry, wrinkly, peels, changes to black, clear marking of healthy/non healthy tissue. spreads slower. not too much swelling wet: venous diseases; infection, moist, swelling skin. no clear demarcation. smells awful. spreads rapidly. bed sores. blood in stasis in limb. |
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inflammation |
non-specific rxn. happens with all types of injury. pain, swelling, redness, heat. sometimes loss of function. it protects the body from further injury, prevents infection and spread of infection, and promotes healing. |
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major steps: |
vascular stage: local : heat, red, swell vasodilation. slows blood velocity and increases blood flow to site. caused by the mast cells degranulating and releasing histamine. increased capilllary permeability: fluid and protien and water and cells ooze out. |
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pattern of response for the vascular phase: |
transient: small inflammatory sustained: more serious. days. delayed: sunburn. |
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cellular response: |
this is systemic. leukocytosis. incr in wbcs. on the scene: 1. neutrophils, 2. monocytes, 3. eosinophils, 4. basophil. |
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neutrophil |
1st to get there but dont last b/c of acidity. phagocytotic. also puts out neutrophil chemotactic factor. like ECF-A, (eosinophil) |
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chemotaxis |
directional movement of cells along a chemical gradient |
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monocytes eosinophils basophil |
turn into macrophages that eat foreign bodies, damaged cells. eosinophil: parasitic infections basophils: like mast cells but circulating. histamine and heparin. heparin is anti-coagulant. prevents too much clotting. |
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plasma derived mediators what are they, what do they do |
all of these secreted during inflammation and activated by enzymes kinins: like bradykinin. most involved kinin in inflam. relaxation of smooth muscle in cap. vasodilation, permeability, PAIN. coagulation/fibrinolysis: development of fibrin. walls off. protects ag. sepsis. complement proteins: vasodil, leukocyte activation, phagocytosis |
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mediators released and produced by the mast cell |
histamine prostaglandins platelet activating factor cytokines |
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histamine |
smooth muscle constriction dilation and permeability of capillaries serotonin (similar to histamine) |
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prostaglandins |
aka leukotrienes. synthesized by mast cell. fatty acids such as PGE 1 and PGE 2 (INDUCE PAIN), and they incr vascular permeability and induce neutrophil chemotaxis. *NSAIDs work by blocking prostaglandins. irritate stomach. In SRS (slow reacting substances) of anaphylaxis, this is the culprit. histamine presynth, secreted 1st, but this synthesized. |
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platelet activating factor |
platelets and fibrin both wall off. activates neutrophils and eosinophils. induces platelets to aggregate. |
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cytokines |
tons of them. polypeptide products like tumor necrosis factor. modulate fn' of other cells, involved in facilitating communication so other cells can do their job. |
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local vs systemic inflammation |
local: redness, heat, pain, swelling, altered function. systemic: fever, pain/muscle aches, lymphadenitis (swollen lymph nodes), leukocytosis, proteins like C-reactive protein (acute phase), erythrocyte sedimentation rate. |
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exudates in inflammatory processes |
serous: blister, watery, clear. no odor or cells. fibrinous: chronic/long term. thick and sticky w/ fibrin. may need to be removed. purulent: like in abdomen.cells. infected. |
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difference betw tissue regeneration and fibrous tissue repair |
regeneration: no scar. epithelial cells just multiply and move in. fibrous: biger wound. collagen and fibrin fill it in. |
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what is primary intention |
some fibrous tissue , but minimal tissue loss and close apposition of wound edges. |
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secondary intention |
significant pressure ulcers. more time, more tissue loss, more fibrin and more collagen , tissue only gains at best 80% of original strength. |
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stages of wound healing |
inflammatory phase, 2-3 days proliferative phase: macrophage recruitment of fibroblasts. epithelialization, wound contraction. form a scar, 3 weeks, remodeling: 6 months.scar fades but gets strong. |
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dysfunctional wound healing |
impaired collagen synthesis: nutritional, lack of protein or scurvy excessive collagen: keloid. dehiscence: pulls apart at suture. strain, sepsis. |
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mechanism of action: viral vs. bacterial |
viral: obligate intracellular bacterial: secrete endo or exotoxisn. gm (-) sepsis: really sick. |
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infectivity |
droplet vs. airborne. ability to get in and multiply |
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pathogenicity |
ability of pathogen to produce disease. smallpox very pathogenic. |
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virulence |
how many viruses or bacteria does it take to cause disease |
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antigenicity |
ability to produce an immune response |
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toxigenicity |
ability to have endo/exotoxins |
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clinical manifestations |
abscess, swelling, purulent exudate fever rash swelling |
