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Tox*4100. UOG > Term One > Flashcards

Term One Flashcards

1
Q

what are four mechanisms that the cell may use in response to cell stress?

A

defend, adapt, conserve, or replace

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2
Q

name some mechanisms that the cell would specifically do in response to cell stress?

A 
manage protein synthesis,
repair dmaage molecules, 
catabolize damage molecules
discard or sequester debris
or cell death
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3
Q

how may a cell adapt?

A

it may induce the gene expression and alter the gene based on activated nuclear receptors.

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4
Q

what happens when a protein is incorrectly folded?

A

they are bound to ubiquitin and degraded in proteasomes or autophagosomes.

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5
Q

what is lipofuscin

A

its dark heterogeneous lipid pigments that accumulate with age. they neurons retain the most, and its the aftermath of autophagocytosis.

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6
Q

what is phospholipidosis?

A

the impaired catabolism of membrane phospholipids by agents that buffer lysosomal pH. immunoreactive lysosome-associated membrane proteins.

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7
Q

what is atherosclerosis?

A

oxidized lipid in phagocytes in arterial walls.

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8
Q

what is the physiological changes in hepatic steatosis (fatty liver)

A

increased mobilization, and increased demand (pregnancy, egg production, insulin deficiency in diabetes, or starvation)

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9
Q

what is degenerative hepatic steatosis?

A

inadequate ATP supply
impaired apoprotein synthesis
impaired lipoprotein secretion

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10
Q

what are some patterns of hepatic steatosis?

A

adipophilin around vesicles

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11
Q

what are membrane blebs?

A

Ca+ influx causes actin filaments contraction and extrusion of organelle-free cytoplasmic blebs

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12
Q

what is the difference between necrosis and apoptosis?

A

necrosis is the enzyme digestion and leakage of cellular concents,
apoptosis is the phagocytosis of apoptotic cells and fragments

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13
Q

what is an example in the human body where tissues have programmed cell death?

A

in the epidermis, where exfoliation (top layer of skin) is actually the dead cells pushed up wards, by the layer on top of the replication layer.

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14
Q

what are some types of insults that may lead to cell death.

A
  1. chaotropic chemical and physical denaturation (thermal, detergents)
  2. resource deprevation (autophagy or cell atrophy)
  3. impaired membrane functions (membrane pores)
  4. death signals (loos of mitochondria, DNA damage)
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15
Q

what is ischemia and hypoxia

A

ischemia (cut of blood flow to tissue)

hypoxia (tissue deprived of oxygen)

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16
Q

what are the four chemical mechanism of cell death

A
  1. covalent binding to functional molecules
  2. ionic interactions with functional molecules
  3. free radical damage to macromolecules
  4. activation of cell death pathways.
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17
Q

what are the examples of free radical damage to macromolecules?

A

membrane lipid peroxidation, nucleic acid breaks, molecular adducts.

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18
Q

what are the two types of activations of cell death pathways

A

intrinsic (DNA damage, mitrochondria damage)

extrinsic (Fas lignand, TNF)

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19
Q

what are the 5 ways cells can die

A
  1. Apoptosis (fragmentatiom, shrinkage, phagocutosis)
  2. Necrosis (cell swelling, membrane leakage, inflamation)
  3. Autophagy (lysosomal catabolism, atrophy, phagocytosis)
  4. Exfoliation (programmed cell death, sloughing)
  5. others
    a) pyroptosis (lysis of infected cells)
    b) Anoikis (apoptosis of detached cells)
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20
Q

within the pidermis what purpose do the dead cells provide?

A

they project basal cells from chemical injury.

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21
Q

what is the processes of the PCD apoptosis?

A
  1. cell fragmentation and rapid phagocytosis of fragments.
22
Q

what are the advantages of apoptosis?

A

there is no leakage of cell content into tissue, it is programmed, and happens have cell breaking into fragments with intact cell membranes, and those phospholipids then flipping.

23
Q

what is the mechanism of DNA damage? (what happens in response?)

A

1.either a strand can break or adducts can interact (R+), the p53 is activated and eiher DNA repair or apoptosis.

24
Q

what happens in necrosis?

A
  1. passive and catastrophic failure of many vital cell functions
    2, lack of ATP
  2. failure of ATP-dependent ion pumps in membranes
  3. leakage of cytoplasmic constitudents
25
Q

what are examples of failure of ATP-dependent ion pumps in membranes?

A 
sodium ion flux (leads to cell swelling)
hydroogen ions (acidosis)
calcium ions moved into cytosol
basically leads to many dysfunction's.
26
Q

what are examples of cytoplasmic constituents

A
  1. serum indicators of necrosis
  2. pro-inflammatory molecules (DAMs)
    this are host responses
27
Q

describe necrosis

A

its the enzymatic digestion and leakage of cellular contents, which follows the acute swelling of cells.

28
Q

what leads to cell swelling>

A

increasing [Na+] and [H+] through a cation channel

29
Q

what leads too cell deat (ion [ ] )

A

increased [Ca++] leads to enzyme leakage

30
Q

what is excitotoxicity?

A

various ligands of NMDA (glutamate receptors activate calcium influx.
low doses=excitation of neurons
high doeses= Necrosis of neurons

31
Q

necrosis can elicit what kind of reponse?

A

inflammatory

32
Q

what is a concern with cell death and inflammation?

A

after cell death, cell leakage of damange-associated molecular paterns (DAMPs) which reacts with receptors on cytokine producing cells (macrophages). this helps alet the immune system to danger.

33
Q

what are some serum indicatiors of necrosis?

A 
for myocardium (Trp1 and CK, increases around 20 hours post)
for Liver (ALT) [levels] increase around 21 following the release, with mg/kg in corn oil.
34
Q

what are a few mechanisms to detect apoptosis.

A

DNA ladders, morphology, blebs, phagosomes, flow cytometry, TUNEL nick end- labbelling with TdT incorporation of dUTP, caspage cleavage, annexin labelling.

35
Q

what are the components of the inflammatory response to the vascular response?

A

hemodynamic responses and microvascular permeability

36
Q

what are the components of the inflammatory response to the plasma protein response?

A

hemostasis, provisional matric for tissue repair, and anti-inflammatory factors to limit the process

37
Q

what are the components of the inflammatory response to the cellular system?

A

platelets, leukocytes, endothelial cells, fibroblasts

38
Q

what are the components of the inflammatory response to the tissue repair

A

phagocytosis/removal of debris
extracellular matrix modification
regeneration of parenchymal/epithelial cells
fibroplasia and angiogenesis

39
Q

what are the 6 basic responses to tissue injury (steps?)

A
  1. hemostais and fibrionolysis (stop bleeding, temporary matrix for healing)
  2. platelet activation and secretion (plug leaks, and initiate tissue repair)
  3. increased blood flow
  4. microvascular permeability (increase supply of cells and proteins)
  5. monocyte recruitment and phagocytosis (remove debris and stimulate repair)
  6. tissue repair (reconstruct or replace damaged tissues)
40
Q

describe hyperemia and congestion

A

hyperemia is increased inflow (arteries vasodilated) happening from exercise/ inflammation?
congestion is decreased outflow (viens vasodilated) caused by local obstructions.

41
Q

vasodilation does what?

A

increases blood flow.

42
Q

during inflammation what can happen?

A

increased blood flow, arteriole/venule dilation, expansion of capitary bed, nutrophil emigration towards blood flow, and leakage of plasma proteins, which leads to edema (increased fluid in bedding).

43
Q

what happens when fibrin is in protein-rich exudate?

A

macromolecular leakage

44
Q

what is the basic responses to tissue injury and necrosis?

A

phagocytic removal of damage cells and tissues

45
Q

what is the rapir responses to tissue injury and necrosis?

A

tissure repair responses in a hematoma (H= fibrin +RBCs

46
Q

how is granulation tissue formed?

A

fibroplasia (fibroblast proliferation) and angiogenesis (endothelial proliferation)

47
Q

what are the additional “specialized” patterns of inflammation.

A
  1. neutrophil infiltration in response to necrosis and/or mucro-orgnanisms
  2. eosinophil and mass cell responses to some allergenic materials
  3. macrophages reponses to peristent matter.
  4. lymphocute responses to antigenic molecules
  5. generalized inflammatory responses due to potent inflammatory mediators in circulation.
48
Q

what is an oxygen-independent injury example/cause?

A

lysosomal proteinases (nutrophil elastase, cathepins)
phospholipases
cationic peptides

49
Q

what is an oxygen-dependent injury example?

A

HOCI- and hydroxyl radicals.

50
Q

name the four types of insults that can cause cell death?

A

chaotropic cheical and physical denaturation

resource deprivation

Tox*4100. UOG (1 decks)

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