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pathology Flashcards

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1
Q

this type of adaptation is an increase in size. -tissue can’t undergo mitosis so this type of adaptation happens

A

hypertrophy

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2
Q

there are 2 types of hypertrophy. what are they and what is an example of each

A

physiologic “normal conditions” -ex. uterus => hormonal activatoin

pathologic “sick conditions” -ex. cardiac muscle to ischemia ex. signals => stretch of cells and changes in protein synthesis alter cell

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3
Q

when the cell is unable to adapt, what route does it take?

A

necrosis or aoptosis

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4
Q

what type of adaptaion has an increase in cell number

A

hyperplasia

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5
Q

what type of adaptation has cell shrinkage

A

atrophy

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6
Q

what type of adaptation is the cell type replaced by another better able to withstand stress

A

metaplasia

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7
Q

what are two types of physiologic hyperplasia?

A

hormonal ex. breast, uterine growth during pregnancy

compensatory -response to removing piece of tissue (liver damage or surgery)-stimulus (growth factors by hepatocytes)

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8
Q

what is pathologic hyperplasia?

A

excessive hormonal/growth factor production -abnormal estrogen/proesterone -wound healing-viral infections

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9
Q

is pathologic hyperplasia usually reversible? are they controlled?

A

yes yes, if stimulus is removed, hyperplasia disappears

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10
Q

what is decreased workload, loss of innervation or blood supply, nutritional deficiency, endocrine deficiency, aging

A

atrophy

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11
Q

how is cell size diminished to maintain survival in atrophy? 3

A
  1. decreased protein synthesis, increased degradation
  2. ubiquitin-proteasome pathway
  3. autophagy
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12
Q

what is the genetic reprogramming of stem cells? what are some examples

A

metaplasia
squamous metaplasia in bronchi, trachea (columnar to squamous bc tougher tissue but loss of functions) (may predispose to metastassi) -chronic gastric reflux (squamous to columnar)

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13
Q

what is the inability to adapt, or continuation of stress/noxious stimuli

A

cell injury and death reversible to irreversible at some point

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14
Q

what are the two types of cell death

A

necrosis

apoptosis

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15
Q

what are the main differences between necrosis and apoptosis

A

necrosis: membrane fragments and release products to extracellular space-leakage=inflammatory response
apoptosis: membrane intact (membrane bleeding) -NO inflammation

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16
Q

what are 6 causes of cell injury

A
  1. oxygen deprivation (hypoxia) -ischemia, pneumonia, anemia, CO poisoning
  2. chemicals in air pollutants, ethanol and etc. (membrane permeability breakdown of punctum system and swelling of cells, osmotic homeostasis, enzyme damage)
  3. infections (sickle cell, enzyme abnormalities)
  4. nutritional imbalance (poor nutrition, obesity)
  5. physical agents (trauma, temperature, radiation, shock, pressure)
  6. aging (replication and repair abilities damaged)
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17
Q

what determines the point of no return

A
  1. mitochondiral dysfunction not reversible2. disturbances in membrane function -there is no definite time when this happens, and after this point everything increases
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18
Q

in necrosis, what is the swelling due to? what are the fatty changes due to?

A

NAME?

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19
Q

what are the changes in the nucleus, the 3 histological patterns?

A

breakdown DNA and chromatin 1. basophilia fades (karyolysis) 2. pyknosis: shrinkage and increased basophilia, the DNA becomes a solid mass 3. karyorrhexis: fragmentation of nucleus. nucleus disappears in 2-3 days cells can go through either one of these, these are not steps

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20
Q

what are the 3 different type of levels in responses to injury

A
  1. tissue levels-necrosis2. cellular levels-nuclear changes; lipid acculmulation3. sub-cellular (molec) lvs- mitochondria changes, cytoskeletal changes etc.
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21
Q

what are the 6 patterns of tissue necrosis

A
  1. coagulative necrosis2. liquifactive necrosis 3. caseous necrosis 4. fat necrosis5. fibrinoid necrosis6. gangrenous necrosis
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22
Q

in coagulative necrosis: -cells are ______ but “outline” is preserved-characteristic of ______ in all tissue (except brain) -no ________ -can go on for a few weeks until the tissue is broken down/phagocytized by _____-persists ______ -structural proteins are _____, enzymes _____

A

NAME?

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23
Q

in liquifactive necrosis: -occurs in brain tissue in response to _____-tissue architecture is not preserved and become a ______-occurs _____-due to _______ and _____ infections - _______ cells

A

NAME?

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24
Q

in caseous necrosis: -destruction of _______-_____ appearance-common in ______-______ cells-pus and _______ like

A

NAME?

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25
Q

in fat necrosis: -from released ______ from pancreas into pancreas and peritoneal cavity -occurs in _____-release of what from exocrine pancrease? -fat destruction by leaked enzymes called…..-liquify membranes of ____ in peritoneum -fatty acids combine w/ calcium = _____

A

NAME?

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26
Q

in fibrionoid necrosis: -occurs in ______-due to abnormal ______ responses-_______ complex deposition in walls

A

NAME?

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27
Q

in gangrenous necrosis: -loss o blood supply to …..-form of ________necrosis and involves many layers: skin and muscles-sometime bacteria becomes involved and is called…..-occurs in people with severe….

A

-limbs-coagulative necrosis -“wet gangrene”-liquefaction by bacteria -diabetes-when the vessels can’t bring oxygen to the limbs

28
Q

the subcellular response to injury w/in a cell are…..

A
  1. autophagy 2. hypertrophy of smooth ER in liver 3. mitochondiral alterations4. cytoskeletal abnormalities
29
Q

autophagy: -_____ digestion of componenets -______ vacuoles -mechinism due to _____ deprevation or stiumuls -can signal ____ if stimulus continues -doesn’t have to lead to …..

A

NAME?

30
Q

what is heterophagy?

A

macrophage injests substance to destroy-ingesting foreign particle and getting rid of it via exocytosis

31
Q

hypertorphy of smooth ER-Smooth ER: _______-abuse to ___ and ____ cause the liver to get bigger to respond to this stimulus -______ hepatocytes

A

-drugs, toxins, metabolism -drugs and alcohol -SER and enzyme P-450 oxidase system -liver hepaocytes: tolerance to drugs and alc-need to increase amounts of drugs for given effect

32
Q

mitochondrial alterations: -increase in _____ and/or _____-megamitochondria (mit become bigger) are in the liver due to ______ -mitochondiral myopathies occur in ____

A

NAME?

33
Q

cytoskeletal abnormalities: -response to ______ stress -______abnormalities -altered motility sperm, cilia, WBC migration -antiproliferative ____

A

-environmental stress. => alterations in intracellular traffic, locomotion and cilia movment (actin), fibrillar acculmulations -microtubular -changes => cells alter so can’t go through mitosis, altered mitotic spindle, use as anti-tumor agents

34
Q

the cellular response depends on the ….the consequences depend on the ….injury results from…..

A

NAME?

35
Q

the causes of the depletion of ATP are…4 thigns

A

reduced oxygen, nutrients, mitochondrial damage, toxins -tissue dependent (liver vs brain, can stand vs can’t stand)

36
Q

the effects of the depletion of ATP are…4 things

A
  1. activity Na/K pump reduced2. increased glycolysis3. influx Ca4. reduced protein synthesis
37
Q

what activates apoptosis of a cell

A

cytochrome c

38
Q

damage to the mitochondria: -sensitivity to ____ types of injury -activate ____pathways

A

-all types of injury -apoptotic pathways (cyt c, leakage proteins to cytoplasm)

39
Q

what is ischemia? -_____ respiration in mitochondria decreases-______ breaks down as oxidative phosphylation decreases, _____ decreases as anaerobic glycolysis increases -blebing: ____ of vesicles bound particles, cells break up into blebs and start leaking its products. what does this lead to

A

NAME?

40
Q

what does the influx of calcium result fro

A

ATP depletoin

41
Q

influx of calcium resulting from ATP depletion: -influx of calcium into the cell and release of calcium from mitochondria due to…-now there is a lot of intracellular ca which activates _____ or _____ -____ increases -cytosolic ca maintained ____x lower

A

-cell injury-necrosis or apoptosis (activate caspases, inc mit permeability -ischemia -10,000x lower

42
Q

pathological effects of ROS -the increases result in ___-occur due to reduced ____-start to react w/ ______ in cell membranes causing the membranes to be reduced, protein synthesis, and DNA degredation -react w/ proteins causing abnormal folding that leads to ______

A

NAME?

43
Q

reactions mediated by free radicals - lipid ____ of membranes -cross linking of …-DNA _____

A

NAME?

44
Q

mechanisms of membrane damage: -increases ____ damages a lot of things and decreases _____ -cytoskeleton damage

A

-calcium, ATP -cytoskeleton damage=> damges the plasma membrane since they are connected. lipid breakdown further breaks down the membrane, due to ischemia

45
Q

examples of cell injuries are…3 thigns

A
  1. ischemia and hypoxic injury2. ishemia-reperfusion injury 3. chemical (toxic injury)
46
Q

ischemia and hypoxic injury are the most ________ of cell injury and can have functional consequences of decrease in _____

A

commonATP

47
Q

ishemia-reperfusion injury have _____&______ infarctions and have recovery of _____

A

myocardial and cerebral infarctions. recovery of blood flow-death of other cells

48
Q

which injury is direct: combine w/ molecule or organelle and can be converted to toxic metabolites

A

chemical (toxic injury)

49
Q

steps in apoptosis: 1. cells recieve _____2. ____condenses and is cut into pieces, cell shrinks, 3. ______ of nucleus and dissolution of nuclear membrane 4. cell ____ up; apoptosis bodies form. macrophages arrives.

A
  1. signal 2. chromatin 3. fragmentation 4. break
50
Q

what are activated to carry out cell programmed death (apoptosis)?

A

enzymes-the membranes still remain intact, phagocytes target apoptic bodies, no leakage from cell

51
Q

apoptosis is both ___ and ____

A

physiologic and pathologic-can eliminate harmful cells, senescent cells (cells that have lived too long)

52
Q

what are teh 6 physiologic cues 1. 2. ______ deprivation3. _____ populations4. cells that served their …..5. elimination of …..6. cytotoxic T ……

A
  1. embryogenesis2. hormone deprivation-endometrial cell breakdown in menstral cycle 3. proliferating populations-intestinal crypt epithelial cell cycles 4. purpose-neutrophils in inflammatory response 5. harmful “self-reactive” lymphocytes 6. cytotoxic T lymphocytes -defense against virus and tumor infected cells
53
Q

the pathologic conditions eliminate cells genetically altered/damaged beyond repair in ……4 things

A
  1. DNA damage (main) 2. misfolded proteins in ER due to ROS 3. infectoin-induce injury4. atrophy due to parenchymal duct clog
54
Q

apoptosis mechanism activate caspase pathways, what are these 2 pathways

A

intrinsic (mitochondrial) which signals increase in membrane permeability, leakage of cyt c extrinsic (death receptor) -lymphocytes that need to be killed

55
Q

in the clearance of cells, the changes in membrane are to promote what? secretion of factors recruit what? prompt what? what receptors recognize apoptotic cells?

A

phagocytosis. phagocytes clearance -thus no leakage macrophage

56
Q

what are the abnormal intracellular accumulatiosn?

A
  1. abnormal metabolisms2. defects in protein folding or transport3. lack of enzyme4. ingestion of indigestible materials
57
Q

what are the 2 abnormal metabolisms?

A
  1. steatoisis: triglycerides-abnormal metabolism, fatty lipids2. steatosis: accumulation of triglycerides -alc abuse, diabetes, obesity, toxins -reversible unless severe
58
Q

metabolism of this is normally regulated. macrophages become filled w/ lipids and due to inherited hyperlipidemia syndromes

A

cholesterol (steatosis)

59
Q

protein reabsorption is due to _______ in kidney tubules; cells try to respond and uptake them

A

excessive leakage

60
Q

glycogen abnormalities is due to ….

A

abnormal metaolism glucose of glycogen, massive stockpiling of glycogen, diabetes

61
Q

are these pigments exogenous or endogenous? 1. carbon2. lipofuscin3. melanin is melanocytes idk why she put this there

A
  1. pollutant (exogenous environment) -lymph nodes, lung tissue 2. endogenous-wear and tear, normal metabolism of the cell -heart, liver, brain, RPE: aging and atrophy
62
Q

what is hemosiderin? what does it have the inability to metabolize? where does it accumulate?

A

pigment derived from hemoglobin. inability to metabolize iron. accumultes in liver cells

63
Q

in chronic inflmmatory skin disesases, macrophages take up…

A

extra pigment

64
Q

pathologic calcification is the abnormal _________. occurs in: -dead/dying tissue known as….-normal tissue known as…

A

deposition calcium salts
distrophic calcificatoin
metastic calcification

65
Q

metastic calcification leads to hypercalcemia: -increased ______ hormone-_____ destruction -vitamin ____ disorder-___ failure-increase ___- in normal tissue

A

NAME?

66
Q

what is known as the decline in proliferative ability, unable to go through mitosis?

A

cellular aging.

67
Q

the exogenous effects of cellular aging cause…

A

DNA damagedefects in DNA repair mechdefects in DNA stabilitizing proteins

Cell Biology (15 decks)

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