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RUSVM Pathology I > Cell Structure And Mechanisms of Cell Injury > Flashcards

Cell Structure And Mechanisms of Cell Injury Flashcards

1
Q

Phospholipids of the plasma membrane?

A

Phosphatidylserine
Phosphatidylcholine
Phosphatidylinositol
Sphingomyelin

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2
Q

What are lipid rafts?

A

Horizontal associations of sphingomyelin and cholesterol

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3
Q

What phospholipid will flips to the outside of the cell signals itself for phagocytosis ?

A

Phosphatidylserine

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4
Q

Plasma membrane components important in cell-cell interactions and cell-matrix interactions

A

Glycoplipids ad sphingomyelin

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5
Q

What are the 4 general arrangements of proteins and glycoproteins?

A

Integral/transmembrane
Linked to the membrane via lipid or cholesterol
GPI-linked protein (glycosylphosphatidylinositol)
Non-covalent associated

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6
Q

__________ creates a hydrophilic pore and permits rapid movement of solutes

A

Channels

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7
Q

__________ binds a solute and undergoes conformational changes to transport solute across the membrane

A

Carriers

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8
Q

What are the two forms of endocytosis ?

A

Potocytosis - caveolate-mediated

Pinocytosis -receptor-mediated (clathrin coated vesicle)

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9
Q

What are the functions of the cytoskeleton

A

Maintain shape
Maintain polarity
Organize the relationship of intracellular organelles
Mobilize

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10
Q

What are the three classes of the cytoskeleton

A

Actin microfilaments
Intermediate filaments
Microtubules

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11
Q

Thinnest filament comprised of globular protein (G- protein) subunits

A

Actin

Muscle contraction and in cell shape/movement

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12
Q

Tissue specific cytoskeleton component that functions in tensile strength, cell shape, signal transduction,regulation of nuclear transcription, ect.

A

Intermediate filaments

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13
Q

Intermediate filament of epithelial cells

A

Cytokeratin

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14
Q

Intermediate filament of mesenchymal cells

A

Vimentin

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15
Q

Intermediate filament of muscle cells

A

Desmin

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16
Q

Thickest cytoskeleton component of a- and B- tubules that function as cables for molecular motor proteins

A

Microtubules

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17
Q

Continuous barrier that is highly resistant to paracellular ion movement and helps maintain cell polarity

A

Tight junctions (occluding junctions)

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18
Q

Attach cells to other cells or the ECM

A

Desmosomes (anchoring junctions).

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19
Q

Mediates passage of chemical or electrical signals from one celll to another

A

Gap junctions (communicating junctions)

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20
Q

Site of synthesis of all transmembrane proteins and lipids

A

ER

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21
Q

Where are ribosomes found

A

Bound to surface of RER

Cytosol

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22
Q

What modifications can be made to proteins in the ER and what mediates this process

A

Oligomerize
Disulfide bonds
Sugar moieties attached

Chaperone molecules retain proteins in ER until all modification ad folding is complete

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23
Q

Where is intracellular calcium sequestered?

A

Smooth ER

Mitochondria

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24
Q

What occurs to proteins in the Golgi apparatus

A

Glycosylation

25
Q

Function of lysosomes

A

Digest macromolecules

Acid hydrolases (tagged with mannose-6-phosphate) are delivered to lysosome

26
Q

Protesosomes identify proteins by ____________ maker

A

Ubiquitin

27
Q

What are the functions of the mitochondria ?

A

Aerobic metabolism
->TCA cycle and election transport chain
Regulate apoptosis

28
Q

What is the Warburg effect?

A

In rapidly growing cells, TCA cycle is used for building blocks on lipid, nucleic acid, and protein -> glucose and glutamate provide carbon=>decreased production of ATP/glucose molecules

29
Q

DNA is wrapped around ____________ to make chromatin

A

Histones

30
Q

What are the 6 mechanisms of cell injury?

A 
Depletion of ATP 
Mitochondrial damage 
CA2+ influx and loss of CA homeostasis 
Oxidative stress
Defect in membrane permeability 
DNA/protein damage
31
Q

What can cause hypoxia/anoxia?

A

Inadequate oxygenation of blood
Reduced transport of O2 in blood
Reduction of blood supply
Blockage of respiratory enzymes

32
Q

A partial reduction in O2 delivery to a tissue

A

Hypoxia

33
Q

No O2 delivery to a tissue

A

Anoxia

34
Q

What infectious agent can cause cell injury??

A 
Virus
Bacteria 
Fungus 
Protozoa 
Metazoan parasites
35
Q

How can immune dysfunction cause cell injury

A

Congenital defect-eg SCID
Acquired defect - viral/chemical/drugs
Autoimmune disease
Hypersensitivity reactions

36
Q

What is the fundamental cause of necrotic cell death??

A

Deletion of ATP

37
Q

ATP is produced by what 2 primary metabolic pathways? What common substrate do they have?

A
  1. Aerobic (TCA)
  2. Anaerobic (Glycolysis)

Glucose

38
Q

ATP depletion can be associated with what two types of injury?

A

Hyopxic

Toxic

39
Q

What are consequences to the cell when ATP is depleted?

A

Na/K ATPase failure -> cell swelling/ ER swelling/ PM damage

Altered cell metabolism -> anaerobic glycolysis -> lactic acid -> increased pH -> loss of enzyme function

Ribosome detachment-> decreased protein synthesis

40
Q

What are the three major consequences of mitochondrial damage?

A

Mitochondrial permeability transition pore

Reactive oxygen species

Apoptotic pathways

41
Q

What is the mitochondrial permeability transition pore and when opened, what occurs??

A

High-conductance channel in the mitochondrial membrane

=> loss of membrane potential -> failure of oxidative phosphorylation -> more ATP loss

42
Q

What are the sources of calcium?

A

Extrinsic

Intrinsic -> SER or mitochondria

43
Q

What can cause accumulation of Ca2+

A

Extracellular Ca increase -> into cell (infectious agent)

Intracellular Ca release -> opening of mitochondrial permeability transition pore (MPTP) and release fro ER

44
Q

Accumulation of Ca2+ leads to activation of what enzymes?

A

Phospholipases - membrane damage
Proteases
Endonucleases - DNA fragmentation
ATPases -breakdown ATP

45
Q

Accumulation of Ca2+ leads to what 3 major forms of damage

A

Membrane damage
Nuclear damage
ATP depletion

46
Q

Reactive oxygen species are normally produced by?

A

Mitochondrial respiration

47
Q

How do ROS initiate autocatalytic reactions?

A

Have and unstable electron configuration

Interacts with adjacent molecules: proteins, lipids, carbohydrates, nucleic acids

48
Q

Oxidative stress leads to what pathological processes?

A

Cell injury
Cancer
Aging
Degenerative disease

49
Q

What is the major producer of ROS in inflammatory reaction?

A

Activated leukocytes (neutrophil and macrophages)

-> destroy microbes and clean up dead cells

50
Q

What causes the formation of reactive oxygen species?

A

Inflammation -activated WBC
Transition metals -donate or accept free electrons
Nitric oxide -chemical mediator/ generated endothelial cells /macrophages / neurons (free radical)

51
Q

How are free radicals removed?

A

Spontaneous decay
Antioxidants- block initiation or inactivate
Storage and transport proteins - transferrin, ferritin, ceruloplasmin
Enzymes- catalase, superoxide dismutase, glutathione peroxidase

52
Q

What are the pathologic effects of free radicals ?

A

Lipid peroxidation in membranes -> extensive membrane damage

Oxidative modification of proteins -> damage active sites, change confirmation, and enhance degradation

Lesions in DNA-> Cell aging, malignant transformation

53
Q

How does lipid peroxidation damage the membrane?

A
  • forms peroxidases->autocatalytic rxn (propagation)
  • ->decreased phospholipid synthesis
  • ->increased phospholipid breakdown
  • -> cytoskeletal abnormalities
  • activation of proteases-> damaged cytoskeleton
  • cells stretch and rupture
54
Q

What is the mode of action of oxidative modification of proteins ?

A

Oxidation of aa side chains, and formation of protein cross-linkages , or oxidation of protein backbone

  • mitochondrial membrane damage
  • plasma membrane damage
  • injury to lysosomal membrane
55
Q

What is the mode of action of DNA lesions for ROS

A

Single stranded or double stranded breaks, cross-linking of DNA strands, formation of adducts

56
Q

How can the plasma membrane be damaged?

A

Reactive oxygen species
Decreased phospholipid synthesis
Increased phospholipid breakdown
Cytoskeletal abnormalities

57
Q

What are the consequences of membrane damage?

A

Mitochondrial membrane damage-> open the MPTP -> decreased ATP

Plasma membrane damage -> loss of osmotic balance and loss of cell contents

Injury to lysosome -> leakage to enzymes -> digestion of RNA/DNA/protein

58
Q

What are the types of protein damage?

A

Accumulation of misfolded proteins
Cells have repair mechanisms for misfolded proteins
When overwhelmed-> proteins accumulated in the ER

59
Q

How is DNA damaged?

A

Radiation, cytotoxic anti cancer drugs, hypoxia

Cells have repair mechanisms

When overwhelmed-> initiates apoptosis

RUSVM Pathology I (17 decks)

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