pod2ndyear's version from 2015-08-23 01:37

celluar rxn to injury overview and adaptations (1.1)


Question Answer
what can happen when there is harm to a cellreversible adaptive changes to a new steady state (hyertrophy, hyperplasia, metaplasia, atrophy) or in cell injury it starts out as reversble then progresses to irreversible
Hypertrophyslow process, increased cell size due to increase protein production.
what mechanisims cause hypertrophymechanincal stress(increased work load), agonists (adrenergic hormones), growth factors(IGF-1)
physiolical hypertrophy"athletes heart" reversible
pathological hypertrophychronic overload (hypertension or valvular disease) irreversible
hyperplasiaincreased # of cells (cell type must be able to divide-not any permanent tissue)
metaplasiainitially reversible. changes due to local stress by reprogramming of stem cells (must have stem cells) via cytokines and growth factors on differentiating proteins. ex.most common is chaning from simle sqamous to columnar-barrett esophagus, respiratory, pancreatic, cervical glands. or like bone growth in tissue-myositis ossificans.
Vitamin A deficiency can cause what type of adaptive changesquamous metaplasia -Keratolmalacia
Vitamin A is needed forocular conjuntiva, upper respiratory passage, urinary tract.
atrophy is a decreased or reduced whatorganells, metabolic need, cell size, number of cells, organ size, fxn of tissue (opposite of hypertrophy and hyperplasia combined)
what can cause atrophydisuse, denervation, decreased blood supply, malnutrition, low hormon
what is it mean by permanent tissuesno stem cells so there can be no hyperplasia. ONLY HYPERTROPHY. ex are cardiac, msk, never
which two adaptive changes often occur togetherhyperplasia and hypertrophy
what is an example of hormonal hyperplasiamammary gland hyperplasia-increased breast cells
what is compensatory hyperplasiaorgan can regenerate after a loss of mass ie partial hepatectomy the liver celss can fill in the gap to original size and fxn.
what is pahtological hyperplasiaexcess hormones lead to excess proliferation of cells which can mutate. risk of CA
what are 2 ways the cell can decrease in sizedecreased protien syn and increased protein degretdation (due to ubiquin degredation and autophagy
if stress continues what can happenmetaplasia then dsplasia (disordered cell growth-reversible at this point), then CA-irreversible

Apoptosis and adaptations

Question Answer
define autophagyself eating. at some point the autosome fuses with lysosomes to breakdown. usefull for misfoled, damaged protiens and microbes
defected autophagyaccumulateds Beta-amyloid peptides (common in alzhimers disease)
what are the intracelluar accumulations (60Lipids, cholesterol, glycogen, pigments, russel bodies, dutcher bodies
lipid accumulations liver, associated with alcohol abuse and diabetics
cholesterol accumulationsatherslerosic plaques. cholesterol granuloma, Xanthomas (familial cholesterolemia)
glycogen accumulationsfound in renal, liver, heart m cells. can cuase cell injury and death. common in diabetes.. leads to nodular glomerulosclerosis
pigment accumulationcarbon from air pollutant found in lympth nodes. leads to anthracosis. tatooing used for colonoscopy. lipofuscin-common in cardiac and hepatocytes. more in elderly. melanin-can form melanocytes. hemosiderin-yellow bron in alveli
russel bodies accumuatiolnwhen plasma cells crank out a lot of antibodies
duther bodiesaccumulation of plasma cells when they make a lo of antibodies
what are 2 types of pathological calcification dystrophic-in dead tissues and metastatic- in normal tissues
biological agingshortend telomerres, reduced protine translation, defect chaperone activity. envronmental-damaged cologen protiens
premature aginghuthinson-guilfor progeria- defective lamin A precursor called progerin.
werner syndrome-mutation of WRN gene cause unwinding of DNA helicase (causes cataracts, hair loss, skin atrophy, ospteoproris, and atheroscleross. increased CA risk, die 40-50)
reasons for phiso apoptosisembryogenenis, homrone dependent, maintain cell number, elimane harmfull, elimate uneeded cells (inflammatroy response)
reasons for pahto apoptosiscells are irreversitly damages-DNA, misfolded, infections
apoptosis is activated bycaspases (proenzymatic). phosphatidlyserine from from inner to outer leafelt anda recognized by phaogcytes. adhesive glycoprotiens are recognied by phags
apoptosis DNA breakdown seen asladder pattern of fragments
most common apoptosis pathwayintrinsic mitochonrial.
others include-
extrinsic by death receptor mediated-Fas ligand activateds caspase 8 and TNF recptor type 1 activates extrinsic apoptosi
Cytotoxic CD8+T cell(perforin)-gransymes activate caspases
intrinsic mitochondiral apoptosis pathwayin healthy cell the BCL2 prevents cytochrome c from leakage aout but when mito damge the cytochrome c leaks out and activates caspases whcih activates apoptosis. Bax-Bak activation to release cytochrom c
what removes apoptotic cellsmacrophages
growth factor withdraldecreases syn of BCL2=activateion of apoptosis
DNA damageP53 accumuates and if DNA damge is irreverisble then P53 triggers apop by activating BCL pro-apotoici protiens (BAX BAK
P53 role in apoptosis if mutated P53 is wont allow apoptosis and so cells can undergo malignant unstopped
misfolede protiensaccumuatlion activates apoptosis. seen in alzheimers, huntings, parkinsons
PArkinsons diseasedepigmination of sustantia nigra
defecive apoposisneoplais, autoimmuni diease
increased apoptsisexcesive cell death-neurodegenerative disease, ishcimic injury, death of vviral infected cells
nectroptosisriggered by TNRF1, caspases not activated, causes swelling and release of contents
prytoisdeat of microes entering cyto, involves csaspass, celluar swelling and realease of contents

Celluar injury 1.2

Question Answer
what are the 6 types of cell injuryphysical, Oxygen deprivation, chemical, infectious, immunolgical, genetic, nutrional
defiine hypoxialow O2 delivery to tissues=low ATP=celluar injury
what are the 3 causes of hypoxiaIshemia, hypoxemia, decreased 02 carrying capacity
what is Ishemiadecreased blood flow either arterial or venous return (bug keria is a syndrom caused by polycythema vera or lupis anticuagulant) athersclerosis
what is Hypoxemialow O2 pressure in blood. can be caused by hypoventilation, difussion defect, right to left shunt, obstructive lung disease, high altitude, increased CO2, COPD, interstitial fibrosis
what is decreased O2 carrying capacitydecreased # RBC or dysfunction of RBC
methemoglobinemiais a hypoxemia issue in that Fe in heme is oxidized to Fe3=cant bind O2. treated with IV mehanine blue
reversible injurycellular swelling=loss of microville, membrane blebbing, RER swelling=ribos pops off=decreased protein syn, nuc chromatin clumping, mylin figures
Irreversible injurymembrane damage=celuar enzyme leak oustide of cell and Ca can rush into cell. and mitochondrial dysfunction(lack of OP=no ATP syn)
irreversible changesbreakdown of DNA, ATP depletion, autophagy, becomes pink and loss of glycogen particles, leakage of celluar contents
why is an inner mito membrane rupture an irreversible injurycells cant repair themselves, (cytochrome c leaks out which activates apoptosis) . with lysosomes- "trash" can leak and combine with Ca which can activete enzymes

cell death 1.3

Question Answer
def pyknosisshrinkage of nuc, pinkish cyto
def karyorrhexisfragmentation of nuc
def karyolysisDNA degredation
def cell deathloss of nuc
what is necrosiscell murder. large group of cells followed by innflamation. patho not phiso
what is apoptosiscell suicide. small group of cells, ATP, programmed cell death.
coagulative necrosisretains structure but nuc disaperars.
ishecmic infarction is what type of necrosiscoagulative (createsa a wedged shaped and pale appearance) or red if bloody and loose
Liquifacfive necrosisliquified appearnce-filled with pus and celluar debri. occurs in abcesses-neutrophils, brain infarctions-microglia and pancreatitis-proteolytic enzymes
Gangreneous necrosiscombination of cagulative and liquifactive. appears mummified. occurs in LE and GI. can have a superimposed infection (liquified necrosis)- wet gangrene
Caseous necrosisappears like cottage cheese. doenst retain architecture . occurs in mycobacteria/fungal and TB
Fat necrosistissue is chalky due to Ca depositis. occurs in pancrease and peritoneal cavity of pancreatitis
fibrinoid necrosisdamage to fribrin within blood vessels. occurs in hypertension or vasculitis.
what are the mechinisms of cell injuryE depletion, mito damage, Ca entry, ROS, membrane damage, protien misfolding
how does E depletion act as a mech for cell injurymito damage doesnt allow for ATP syn due to OP not working in mito. other ATP pathways downstream can be affected by toxins ect.
connect ishemia with down the road issuesmito damage=no OP= no ATP=
1 disrupts the NA/K pump: alllows Na into cell which allows water to follow and the cell will swell/blebbing
2 no OP=anerobi glycolysis=lactic acid=clumoing of nuc chromatin
3: no ATP=detachment of ribos=decrease in protine syn, protein misfloding, nuc membrane damage=necrosis=lipid deposition
how does mito damage act as a mech for cell injurycan cause mito permeability transition pore=decreased ATP, leakage of cytochrom c that can activate caspases that can activate apoptosis
how does loss of Ca homeostasis act as a mech for cell injurydamage mito and ER allow for Ca to escape into cytosol=can activate enzymes (phospholipaes, proteases, endonucleases). also increased mito permealbiity can activate caspases
how does Oxidaive stress act as a mech for cell injuryfree radicals initiate autocatalytic rxns=loss of steady state=oxidative stress
how are ROS (reactive oxygen species) made (equation)inflammation--bursts of ROS, radiation-water into OH and hydrogen free radicals chemicals, reperfusion injuryalong with incomplete reduction and create: superoxide...hydrogen peroxide...hydroyl radical...2H2O
how are the ROS taken care ofsuperoxide-SOD (superoxide desmutase), hydrogen peroxide-catalase, hydroxy radical-glutathione peroxidase (fenton reaction???)
what is an example of a free radical injuryCCL4...via P450...CCL3 in liver=celluar swelling=ribos detach= no protein sysn=decrease apolipotiens= fatty changes in the liver
why is nitric oxide a problem ROScan react and become highly reactive peroxynitrite anion
effects of ROSdisruption of plasma membrane organells, abnormal folding, mutations in DNA
what is a reprofusion injuryreturn of blood to ishemic tissues=O2^- = increased cardiac ensymes like tropoinins. after reprofusio of infarcted myocardial tissue
how does membrane disruption act as a mech for cell injuryROS, decreased phospholiid syntheis, increased phospholipid break down, protease activation. membrane damage is a consistant feature of most forms of cell injury
how does damage to DNA/protiens act as a mech for cell injurydamage to DNA=creates misfoled protines=apoptosis