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117 Cards in this Set

  • Front
  • Back
what are some examples of adaptation to cell injury?
which modes of adaptation are reversible?
dysplasia (?)
which mode of adaptation is usually NOT reversible?
dysplasia (?)
what is the process that results in involution?
decrease in cell number
differentiate b/w agenesis, aplasia, and hypoplasia
agenesis- complete absence of organ AND its primordium
aplasia- absent organ due to failure of dev of its primordium
hypoplasia- underdevelopment of an organ w/ decr # of cells
what are 2 general mxns of atrophy? exs?
atrophy can be physiologic (hormonal, compensatory) or pathologic (XS hormone stim or GF)
what are some causes of pathologic atrophy?
disuse, denervation, decr blood supply, poor nutrition, loss of hormonal stimulation, aging, pressure
is organ atrophy due to reversible or irreversible cell loss?
atrophy of cells can lead to atrophy of organ
aplastic anemia
marrow failure
pancytopenia (anemia, neutropenia, thrombocytopenia)
suppression/disappearance of m
what are some examples of physiologic atrophy?
embyogenesis: notochord, thyorglossal duct, lg vessels of CV system
decr size of thymus
why does the heart take on a brown pigment with age? what else happens?
atrophy of heart; decr cellular components->deposits of residual material (lipofuscin granules)
mxns of atrophy
active process
decr cell size/fxn to adapt- decr activity of cell
removal of organelles and macromolecules by autophagy
what are some processes involved in atrophy?
decr in transcription genes
incr proteasomes
decr protein elongation
how do cells reduce activity and atrophy to adapt?
downreg protein syn
incr protein breakdown: ubiquitin-proteasome (ubiquitin recycled)
how does autophagy contribute to atrophy?
organelles surr by ER mbr->autophagic body
fuses with lysosome
digestion by acid hydrolases
residual body left with undigested materials
what does a residual body contain?
dense, undigested material in cell
how can you tell the difference b/w atrophy and hypoplasia of an organ? (1 kidney)
hypoplasia- supplying blood vessel is also smaller
opposite kidney is larger than usual
what are some charac of hypertrophy?
incr in cell size
when hypertrophy (w/o hyperplasia) can be due to cells unable to divide
due to increase in cellular structures
NOT due to swelling
what are some ex of reversible cell injury?
morphologic changes:
hydrophobic, fatty, hyaline degeneration (mallory bodies), inclusions and deposits
what are some ex of irreversible cell injury?
hyperplasia of endometrium: appearance and prognosis
sawtooth endometrial glands
incr chance of becoming a carcinoma
what is more likely to become malignant: neoplastic or hyperplastic polyp?
polyp-adenoma; growth of glandular tissue
what are some ex of physiologic hyperplasia/hypertrophy?
estrogen stim of endometrium: proliferating gland epithelium and stroma (with BV); glands elongate, more complex (can dev carcinoma)
hormone changes w/ pregnancy
regeneration of liver
pathologic hypertrophy and hyperplasia
incr wkload for heart->hypertrophy
chronic renal failure->low Ca2+->parathyroid hyperplasia
remove kidney->compensatory hypertrophy of other
myocardial hypertrophy: why and what limits it?
ex: with HTN
allows heart to meet CO demand
limited by its own blood supply
describe the process of myocardial hypertrophy
break down (proteasomal) cell components not req
what are some ex of genes who expression is altered in myocardial hypertrophy?
induce embryonic genes- (ex: beta myosin replaces alpha b/c beta uses less ATP); reinduce ANF (diuretic to decr afterload)
what do kinases that inhibit cell death result in?
what is metaplasia? is it reversible?
change in one mature cell type to another
forms tissue thats not normally present
reflects change in environ for which tissue isnt suited
yes, reversible
ex of metaplasia
barrett's esophagus:
transition from esophageal stratefied squamous to columnar
chronic acid reflux
risk: adenocarcinoma
what is the most common epithelial metaplasia?
columnar to squamous
resp tract due to chronic irritation (smoking)
loss of mucus secretion
what is a complication of metaplasias?
often the influence that induces metaplasia can induce malignant transformation when persists
ex: adenocarcinoma from Barrett's esophagus
ex of squamous metaplasias
transition into stratified squamous:
bronchial mucosal pseudostratefied columnar (cigarettes)
transitional epithelium of bladder (stones)
epithelium lining exocrine, bile ducts (lodged calculi)
mxn of metaplasia; what is it NOT?
reprogrammed stem cells (locally prod GF, cytokines)
in areas of chronic inflamm (inflamm cytokines)
NOT a phenotypic switch
what is dysplasia?
abnorm maturation of cells in a tissue; loss of uniformity and orientation of cells
often indicative of early neoplastic process (cancer-like changes)
what are some etiological agents of cell injury? (8)
hypoxia, physical and chemical agents, infection, immune rxn, genetics, nutrition, aging
what are some things that happen when cells are injured?
depletion of ATP
generate ROIs
defective membrane permeability (mt, lysosome, plasma mbr)
incr intracellular Ca2+
what are the essential cellular components? (4)
aerobic resp
cell mbrs
protein syn
(all targets of cell injury)
2 classes of cell injury and their properties
reversible- change in ion flux and water influx-> reduced ox P, ATP depletion, cellular swelling
irreversible->cell death:
necrosis and apoptosis
are necrosis and apoptosis pathologic processes?
necrosis-always pathologic
apoptosis-sometimes pathologic; sometimes normal (development)
why do is there a decreases in basophilia in irreversible cell injury?
loss of ribonuclear proteins
what are 4 ex of reversible cell injury?
cellular swelling (hydropic change)
fatty change (liver)
hyaline degeneration
inclusions and deposits
what are mallory bodies?
"alcoholic hyalin"
eosinophilic intracytoplasmic inclusion in liver cells
composed mainly of keratin
what are 4 locations of subcellular changes in reversible cell injury?
ER-dilation; allows for better detox
mt-swelling, small phospholipid rich amorphous densities
PM-blebbing, distortion of microvilli, lose intercellular attachments
nucleus- disaggregation of granular and fribillar elements
what does a "hyaline" change refer to?
alteration in cells or ECM
gives glassy, pink appearance (H&E)
what are some reversible cell changes that occur in hypoxia?
low ATP->decr transport syst->water, Na+ influx->cell swelling
decr ox P->incr glycolytic->incr lactic acid->decr pH->alter enzymes
decr protein syn (ribosomes detach)
alter cytoskel
decr cell fxn
what are the stages the nucleus goes through in necrosis?
nuclear condensation (pyknosis)
nuclear fragmentation (karyorrhexis)
nuclear dissolution (karyolysis)
what happens in the mt with cell injury?
open MPTP- inner mbr; dissipates proton motive force and ox P
rel of cytochrome c->apoptosis
when is cell death inevitable?
loss of ATP syn (irreversibe mt damage)
impossible regulation of intracellular components
what happens with uncontrolled Ca2+ influx?
Ca2+ activates ATPases, phospholipases, proteases, endonucleases
what are enzymes rel that allow us to know where the cell damage is occurring?
AST, ALT- liver
creatine kinase, troponin- heart
lipase, amylase- pancreas
what are morphological changes that occur in irreversible cell injury? when can they be detected?
mt- swelling, form dense bodies of Ca2+
lysosomal enzymes rel->digest cell contents
nucleus-pyknosis, karyorrhexis, karyolysis
6-12 hours after cell death
what are the general mxn of reperfusion injury?
incr O2 free radicals
activated C'
cytokines->vasoconstriction, adhered inflamm cells
what is an enzyme that is produced in reperfusion injury that contributes to cell death?
xanthine oxidase: converts hypoxanthine->uric acid (2 steps) and produces radicals
what causes free radical formation? (5)
1. radiation
2. enzymatic chance of chemicals
3. redox rxns
4. Fe2+ and Cu2+ (as catalysts)
5. NO (forms peroxynitrite)
what is the fenton rxn?
forms hydroxyl radical
Fe2+ (ferrous) plus peroxide -> hydroxyl radical plus Fe3+
Fe2+ regenerated by superoxide
what is the Haber Weiss reaction?
peroxide plus superoxide -> hydroxyl radical
what is an example of enzymatic changes in chemicals that form free radicals?
P450 mixed fxn oxidases in SER (esp liver), in an attempt to detox CCL4 and acetaminophen prod highly toxic metabolites
how do free radicals damage the cell?
lipid peroxidation (phospholipid)
crosslinking of proteins
ss DNA breaks
what is esp damaged in the rxn b/w CCL4 and P450?
RER-inhibits protein syn
no apoprotein syn, no lipid export-> fatty liver
what is the seq of events that leads to fatty changes and necrosis in the CCL4 toxicity?
lipid peroxidation-> autocatalytic formation of new radicals

influx of Ca2+->necrosis

fate of the cells depends on the amount of free radical formed
how do we prevent free radical damage?
antioxidants: vit E, A (retinoids)
sequester molecules that promote prod of free radicals (transferrin, ferritin, ceruloplasmin)
how does NO prevent free radical formation? what is odd abt this?
decreases uptake of cellular Fe by transferrin
NO also CAUSES free radical formation
detoxifying enzymes
SOD (mt-Mg; cytosol-Cu/Zn)

catalase (peroxisomes)

GPX (mt and cytosol)
types of necrosis
enzymatic fat necrosis
coagulative necrosis
ex: MI
denaturation of cell proteins; cell architecture preserved for some days
characteristic of hypoxic death of cells in all tissues except brain
histpathology of coagulative necrosis
coagulated, anucleated
basic structure retained
edema and inflammatory cells
area of organ with coagulative necrosis due to ischemia
what are the 2 appearances of an infarct?
pale/anemic- ex: heart; single blood supply
red/hemorrhagic- ex: lung; dual blood supply or lg amt loose CT (bronchial,pulmonary aa)
what is hyperemia seen around an infarct?
due to inflamm resp and dilation of vessels around infarct
which type of infarct will occur with a small decrease in blood supply? (subendocardial or transmural)
subendocardial- systolic squeeze
begins as ischemia to distal extremities
->coagulation necrosis
->liquefactive necrosis with bacterial superinfection of necrotic tissue (wet gangrene)
liquefactive necrosis
usually due to bacterial or fungal infections (activate inflamm resp)
complete digestion of dead cells->focus of white cells and cell debris/liquid, viscous mass
ex: abscess
what happens if liquefactive necrosis was initiated by acute inflamm response?
cell debris in yellow, creamy PUS (w/ dead white cells)
what is the exception to liquefactive necrosis?
hypoxic death of cells (which usually causes coagulative necrosis) in CNS causes liquefactive necrosis
fat necrosis
areas of fat destruction
ex: acute pancreatitis, alcohol, gallstone in sphincter of Oddi
rel of pancreatic enzymes (lipase)-> digests TAGS rel FFA;
FFA + Ca2+ -> saponification
how does fat necrosis appear grossly and microscopically?
grossly: chalky, white areas (basophlic Ca2+ deposits)
adipocytes lose nuclei, blue discoloration
caseous necrosis
mycobacterial or fungal infection
"cheesy" grossly
no residual cell structure
surrounded by Mph and fibrosis
how does caseous necrosis appear on LM?
amorphous, granular debris;
composed of fragmented, coagulated cells within distinct inflamm border
giant cells
fibrinoid necrosis
bright pink on H&E
in arteriolar walls
HTN or IC deposition
necrosis and damage of vessel
what are 2 examples of diseases that may result from abnormalities in apoptotic processes?
pathologic processes involving apoptosis
some viral diseases (councilman bodies)
atrophy of organs after duct obstruction
normal processes involving apoptosis
homeostatic mxns: in untero dev, involution of endometrium in menstruation cycle
destroy host cell: virus-infected, damaged DNA, downreg immune cells
3 groups of caspases; targets?
interleukin converting enzyme (ICE)-like: cytokine production
initiator caspases (2,8,9)
executioner caspases (3,6,7)
targets: activate DNase, DNA repair enzymes
2 modes of apoptosis initiation
extrinsic: TNF; generate active caspases (inducers0; Fas/FasL
intrinsic: replace anti-apoptotic proteins (remove inhibitors); form leaks in mt
examples of when intrinsic pathway active
involution of endometrium
castration->cell loss in prostate
what is a councilman body?
eosinophilic globule found in liver cell of ppl w/ yellow fever...each body~ apoptotic event of 1 liver cell
also seen in acute hepatitis
necrosis vs. apoptosis (size, nucleus, PM, contents, inflamm, role)
necrosis: swelling, non-specific breakdown of DNA, PM disruption, contents leak, INFLAMM, pathologic

apoptosis: shrink, fragmented nucleus, PM intact, contents rel in blebs, NO INFLAMM, normal or pathologic
heterophagy vs. autophagy
hetero: endocytosis of extracell material
auto: digestion of old organelles
both involve lysosomes
what are residual bodies?
lysosomes with undigested material
what is lipofuscin?
pigment granules represent undigested material remaining from intracellular lipid peroxidation
what happens to the number of mt in a hypertrophic vs atrophic cell?
hyper-incr number mt

atrophic- decr number mt
what is a megamt? where do we see it?
lg, abnorm shape
alcoholic liver disease
SER in cell injury
may hypertrophy
incr detox abilities (also with barbituates)
req higher doses of drugs
mxns of intracell accumulations (6)
inadequate brkdown
inadequate packaging, transport, secretion
abnormal protein can't be metabolized
mutation->inactive enzyme
injury-> altered intracell component can't be broken down
abnormal exogenous subst taken up b/c can't be broken down
lysosomal storage diseases are ex of what type of mxn for intracell accumulations?
genetic mutation-> inactive enzyme
accumulate intermediates
mallory's hyalin is an ex of what type of mxn for intracell accumulation?
injury-> acquired alteration of intracell component that cant be removed
fat accumulation
begins as small droplets (microvesicular)
coalesce into one lg droplet (macrovesicular)
what are 2 ex of disease where we only see microvesicular fat accumulations?
Reye's syndrome- kid with flu-like sx given aspirin
acute fatty liver of pregnancy-3rd trimester; can be fatal to mother; disordered metab of FA in mt of fetus
what are foamy cells?
MPh stuffed with cholesterol
imp in atherosclerosis
what is alpha-1-antitrypsin disease?
accumulation of abnorm folded A1AT in liver cells
can't be exported or metabolized
liver damage
absence of protein->emphysema (can't inhibit elastase)
what is hemosiderin?
golden brown pigment granules in cells that develops from ferritin when there is XS Fe
stains blue with Prussian blue
transferrin vs. ferritin
transferrin-specific transport proteins for Fe
ferritin-Fe storage form in cells
how is Fe excreted?
it isnt; no physiological route
XS Fe->free radicals, damage DNA, stim collagen syn
cond with Fe accumulation
abnorm RBCs or incr breakdown:
aplastic anemia
sickle cell
BM transplant
where does Fe accumulate with incr RBC breakdown?
incr uptake of Fe in GI
deposited and organs->toxicity
(liver, pancreas, skin, gonads)
inflamm rxn in liver can lead to cirrhosis and neoplasia
how is copper excreted?
biliary tract
obstruction -> Cu accumulation in hepatocytes
what is wilson's disease?
inability to excrete Cu from hepatocyte-> accumulation
Cu deposited in tissues (liver, brain, eye)
Kayser-FLeischer rings: eye lesions, green/brown deposits
what is anthracosis?
accumulation of carbon that blackens lungs
inhaled carbon picked up by kupffer cells and is taken to regional LN
wear and tear pigment
indicates free radical injury and lipid peroxidation
liver and heart
incr with age
where do we see pathologic calcification?
calcific bodies in irreversibly injured mt
dystrophic calcification
metastatic calcification
what is dystrophic calcification?
Ca deposited in necrotic or chronically traumatized tissue
*normal serum Ca
exs of dystrophic calcification
fat necrosis (saponification)
coagulation or caseous necrosis
deposition on heart valves (aortic)
metastatic calcification
*high serum Ca
deposits in VIABLE tissue
causes: incr PTH, brk down of bone, vit D intox, renal failure
what is tissues/organs are usually affected in metastatic calcification?
* esp when assoc with alkaline mileu
-interstitium of gastric mucosa
hyaline vs hyalin
hyaline- adjective for pink; intracell or extracell

hyalin- noun; subst with hyaline appearance; intracell