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141 Cards in this Set
- Front
- Back
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3 cell reactions to stress
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adapt, reversible or irreversible injury (cell death)
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6 causes atrophy
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decreased workload, hormonal or nervous stim, nutrition, blood supply, or aging.
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hypertrophy causes
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physiologic or pathologic - response to hormone, workload, or limited adaptive response: L.ventricle hypertrophy.
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02 deprivation
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Hypoxia
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loss of blood flow
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Ischemia
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tissue injury time in ischemia vs. hypoxia
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ischemia injures more quickly, compromises avail. of metabolic substrates
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causes of cell injury
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O2 deprivation, physical agents, chemical, infectious agents, genetic disorders, nutritional imbalance
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change of a differentiated cell type to another
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metaplasia - response to persistent (chronic) injury
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2 common chronic injury cell type changes
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smoker:ciliated epithelium - stratified squamous. Cervix - glandular to squamous epithelium
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4 systems in cell vulnerable to injury
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membrane pump, genetic apparatus, aerobic respiration, structural-enzymatic proteins
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4 mediators - cell death
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02 and 02 free radicals, intracellular Ca+, ATP depletion, membrane permeability defects
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most common cause of cell injury and the tissue result
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hypoxic ischemia - coagulative necrosis
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2 energy mechs affected in cell injury
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aerobic respiration (oxydative phosphorylation), glycolysis (anaerobic respiration)
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result when each energy mech. injured
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aerobic - ATP production lost. glycolysis - depletion of glucogen, byproducts and acidity
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byproducts - glycolysis
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lactic acid, reduces intercellular pH
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mechanisms of injury - ischemia
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ATP depletion, Na+-K+ pump stops working,Potassium leaks, sodium stays, cell swells. ribosomes detach, protein synthesis slows, lipid accumulates, nuclear chromatin clumps
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3 factors IRREVERSIBLE cell injury
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massive amounts Ca+, mitochondria covered, ATP production lost. Cell membrane leaks, lysosomes leak. Enzymes digest cell components.
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2 diffs - reversible vs. irreversible injury
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CELL MEMBRANE DAMAGE - most important (integrity) Can’t reverse mitochondrial damage (no energy)
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4 mechanisms free radical injury
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peroxidation of membrane lipids, DNA breaks, X-linking of proteins destroys function, damage to mitochondria.
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6 free radical injuries
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reperfusion/hypoxia, aging, radiation, 02 toxicity, chemical injury, INFLAMMATION
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2 mechanisms chemical injury
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direct (chemotherapy), toxic reactive metabolite reaction (in liver)
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2 morpological signs REVERSIBLE cell injury
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SWELLING, fatty change
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imp. cause of liver damage
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hepatotoxin - ALCOHOL - causes incr. fatty synthesis
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inflammatory cause of free radicals
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produced to kill bacteria
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5 types necrosis
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COAGULATIVE, liquefactive, caseous, gangrenous, fat/enzymatic
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necrosis type determinants
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cell type and cause of death
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2 methods necrotic cell removal
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denaturation, enzymatic digestion
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3 changes to nucleus in cell death
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shrinkage, fracturing, disappearance
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indicator of nucleus shrinkage - cell death
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increased staining
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nuclear shrinkage
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pyknosis
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nuclear fragmentation
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karyorhexix
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nuclear disappearance
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karyolysis
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many cytoplasmic proteins denature - result?
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cytoplasmic eosinophilia (incr. staining)
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coagulative necrosis histology
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well demarcated - determined by blood supp.
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dead cell structure - coag. nec.
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eosinophilic ‘tombstone’ architecture there, nucleus not
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liquefactive necrosis cause
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enzymatic digestion cell architecture/lysosomes, enzymes released
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usual cell death cause - liquefactive necrosis
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bacterial
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markers of infarct in brain
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cyst, tissue debris, fluid, inflamm. cells, bacteria
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necrosis - comb. liquefactive/coagulative
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caseous. granular, eosinophilic debris
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disease assoc. w. caseous necrosis
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tuberculosis
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normally seen in caseous necrosis
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granulomatous inflammatory border with giant cells, epitheloid histiocytes
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adipose necrosis
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fatty enzymatic necrosis in adipose tissue - assoc. w/calcification
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location/cause fatty necrosis
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peripancratic (sometimes mesenteric) acinar cell damage, lipases released, calcification --calc.soaps
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liquefactive or coag. necrosis of limbs called
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gangrene - wet or dry (eg diabetes)
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apoptosis result
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nuclear disintegration, DNA cleavage
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2 conditions assoc. w apoptosis
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viral infections, radiation injury
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fast necrosis dev. in organs with?
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high met. rate (int. mucosa), cytolytic enzymes(pancreas), vital organs - high O2 (brain, heart, lungs)
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hypertrophy seen in cells which
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can’t divide
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hyperplasia occurs where
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cells capable of mitosis
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physiologic hyperplasia 2 types, examples
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compensatory (liver regen) hormonal (breast/uterus - pregnancy)
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metaplasia
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reversible change of one differientiated cell type to another
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metaplasia results from
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common response to chronic injury/inflammation/irrit.
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physiologic adaptation feature
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cells tissues modify to new demands
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pathologic causes of apoptosis
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viral infection, radiation injury
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physiologic causes of apoptosis
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embryogenesis, hormonal (breast), proliferating populations (lymph)
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inflammation is
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reaction of living tissue to injury
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inflammation can result in
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tissue damage
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inflammation mediators
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chemicals derived from host
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inflammatory changes occur where
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terminal vascular bed, blood, conn. tissue
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main cells involved in inflammation
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monocytes, neutrophils, macrophages
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purpose of inflammation
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eliminate injurious agent and initiate repair, restoring continuity if not function
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clinical symptoms of inflammation
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rubor, calor, dolor, tumor, loss of function - redness, heat, pain, swelling, loss of funct.
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characteristics acute inflam.
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short duration, fluid exudate, plasma proteins (edema), neutrophile and leukocytes to tissue, then macrophages.
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2 poss. outcomes acute inflammation
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resolution or complications (progress to chronic)
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chronic inflam. char.
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long duration, lymphocytes, plasma cells, macrophages, vascularization, fibroblasts.
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tissue type assoc. w chronic inflam
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granulation and connective
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scarring problem/consequence
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diminishes tissue function, can lead to organ dysfunction (and death)
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limiting factor of inflammation
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only at site of injury
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2 ways injurious agent isolated in inflammation
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encapsulation (fibrous capsule) intercellular storage(engulfment - phagocytosis and storage.)
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1st vascular chgs in inflammation
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momentary vasoconstriction (reflex) followed by vasodilation - incr. blood flow, then congestion - filled w/ blood.
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vasodilation and congestion cause
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redness, heat.
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following vascular chgs
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blood tissue barrier chgs - widen endothelial gaps - histamine reaction - edema
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swelling of inflammation bc of
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capillary leakage - blood plasma and leukocytes to tissue
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inflammatory exudate
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cellular debris, plasma proteins, fluid
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cellular events of inflamm
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margination, pavementing w/in vessel wall, emigration from vessel to interstitium, chemotaxis-site, phagocytosis
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inflamm cell types
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Neutrophils first 24 hrs, then monocytes 24-48 hrs
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exudate specific gravity
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1.02
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5 host derived main mediators inflammation
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vasoactive amines, plasma proteases, cytokines, adhesion molecules, arachiodonic acid metabolites
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2 vasoactive amines
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histamine, seratonin
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purpose, origin vasoactive amines
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vascular chgs inflammation
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what produces vasoactive amines
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mast cells, platelets
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3 systems of plasma proteases
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kinin, clotting, complement systems
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kinin sys assoc. w?
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pain
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cytokine, peptide source
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macrophages
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cytokine purposes
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inflammatory mediators (IL1, TNF), activate polymorphs, macrophages to incr. killing, incr. vasc. permeability
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ICAM1 def
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cytokine - initiated production by endothelium
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ICAM1 purpose
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facilitates inflam cell binding to vessel endothelium
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AA metabolites are?
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arachiodonic acid - degraded phospholipids of cell membranes
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AA’s cause?
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inflammation - vasodilation, chemotaxis, increase vasc. permeability
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2 anti-inflam drugs
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aspirin, steroids
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NSAIDS
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non steroid anti inflammatory
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aspirin function
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blocks prostaglandin synthesis
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prostaglandin function
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pathogenesis of pain and fever - hyperalgesic
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steroid function
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blocks prostaglandin, leukotrines
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leukotrines
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chemotactic, activate neutrophil aggregation and adhesion
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chronic inflam cells
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MNL, lymphocytes, plasma cells
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main processes, chronic inflam
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healing and repair and tissue destruction cycle
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define granuloma
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form of chronic inflam w/ lots of histiocytes, giant cells, LANGHANS cells
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granuloma forms bc
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bacterial or fungal infection, foreign materials
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2 results of tissue dmg
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regeneration if same tissue type, or scar repair
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purulent exudate
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PUS proteins, neutrophils, cell debris: liquefactive nec
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walled off localized pus collection
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abscess
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acute vs chronic characteristics
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fluid protein exudate and neutrophils versus tissue dest. and repair, lymphocytes, macrophages and chemical mediators for vaso/cellular response
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4 vascular events of acute inflam
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transitory reflex vasoconstriction - vasodilation - incr. bl.flow - capillary permiability incr.-fluid to interstitium= swelling, stasis, incr. blood viscousity, leukocytes enter
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problem w phagocytosis in inflam
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lysosomal enzymes to extracellular sp - cell/tiss. dmg
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4 outcomes acute inflam
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resolution, scarring, abscess, progress - chronic
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results of AI resolution
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little injury or destruction, normal function
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scarring in nonregen tissue result
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loss of function (deadly in cases: heart, brain)
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3 examples persistent infections causing chronic inflam
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tuberculosis, syphilis, fungi
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4 causes of chronic inflam
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persistent infection, delayed hypersensitivity react., toxic agent exposure (inorganic metals), autoimmune disease
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2 autoimmune disorders assoc w chronic nflamm
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rheumatoid arthritis, thyroiditis
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chronic inflammation: granuloma histology
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activated macrophages, large squamous cell epitheloid appearance
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3 morphologies inflammation
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serous(watery, few proteins), fibrinous, purulent(neutrophils, necrosis, edema, pyogenic orgs).
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pyogenic organism example
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staphlococcus
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abscess characteristics
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fibroblastic surround (early repair) w/ pus, pyogenic organisms, central necrosis
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eroded necrotic epithelium
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ulcer - assoc. w acute and chronic inflam
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3 systemic effects inflam
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fever, elevated WBC count, neutrophylia, lymphocytosis
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exudate with fibrin
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fibrinous
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exudate with RBCs
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hemorrhagic
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exudate - yellow/green
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purulent
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clear exudate
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serous (plasma) - edema
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cause of pain assoc. w inflamm
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pressure on nerves, and chem. mediators
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inflammation is
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response of VASCULARIZED tissue to injury
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inflammation designed to
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bring plasma proteins to site of injury in fastest poss.time
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main chgs in inflammation
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blood flow changes, formation of fluid and cellular exudates
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3 functions fluid exudate
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bring plasma proteins, dilute toxins, loosen conn. tissue to allow diffus-migration of cells to injury site
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cell type assoc w/ parasitic infection
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EOSINOPHILS
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PMN
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polymorphonuclear leukocytes: NEUTROPHILS
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chemical attractants at injury site
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host factors - plasma proteins, and infectious agents
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protein expressed on infectious agent
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OPSONIN - labels agent for phagocytic destruction
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possible outcomes acute inflammation
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resolution, abscess, tissue dest., systemic involvement, progression to chronic
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3 conditions lysosomal enzymes released inadvert. during inflamm.
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during phagocytosis, trying to digest on flat surface (frustrated phagocytosis), cytotoxic release
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result of lysosome enzyme release
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tissue destruction
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result of tissue dest
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catastrophic if in heart, valves, major vessels
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flat surf. destruction of what by neutrophils
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AgAb complexes
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system: removes AgAb complexes in spleen, liver, bone marrow
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reticulo-endothelial system
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autoimmune disease def
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antibodies against self
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if AbAg complexes in body for too long?
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acute inflamm response, neutrophils - injury site
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frustrated phagocytosis in kidney, joints, heart
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glomerularnephritis, arthritis, carditis
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tissue destruction from cytotoxic release
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GOUT
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cytotoxic release
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neutrophils phagocytose particles harmful to them, burst, releasing enzymes, destroy tissue.
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