Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Foundational toolkit III - wk1 > cell injury and death > Flashcards

cell injury and death Flashcards

1
Q

what are the 9 causes of cell injury

A
  1. physical agents
  2. infectious agents
  3. immunologic dysfuntion
  4. genetic derangements
  5. nutritional imbalances
  6. workload imbalances
  7. chemicals, drugs, and toxins
  8. aging
  9. 0xygen and energy deprivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cell injury

physical agents

A
  • heat, cold, radiation, electric shock
  • may directly rupture cells, damage their blood supply, denature cell proteins, create free radicals, or damage DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cell injury

infectious agents

A
  • viruses, prions, bacteria, rickettsiae, protozoan, metazoan parasites
  • damage cells by directly invading the cells or producing toxins, or the damage may be due to the inflammatory reaction they induce
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cell injury

immunologic dysfunction

A

failure to respond to infectious agents and other antigens as a result of congenital or acquired immunodeficiencies; autoimmune dieases; hypersensitivity reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cell injury

genetic derangements

A
  • mutations
  • cause a wide spectrum of abnormalities, from gross defects that are incompatible with life, to subtle variations in susceptibililty to other diseases; hypersensitivity reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cell injury

nutritional imbalances

A

include decreased food intake (starvation) excessive ingestion of calories leading to obesity, and deficiencies or excessive intake (toxicity) of vitamins and minerals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cell injury

workload imbalances

A

due to excess or deficiencies of either physical activity or hormonal secretion and often cause apoptosis, atrophy or hypertrophy/hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cell injury

chemicals, drugs, and toxins

A

act by a variety of different mechanisms to lead to cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

cell injury

aging

A

aged cells may suffer a lifetime of DNA damage and/or accumulation of cellular debris that interfaces with normal cell functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how long does it take to notice microscopic changes associated with cell injury

A

6-12 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how long does it take to notice gross changes associated with cell injury

A

hours-days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the 5 mechanisms of cell injury

A
  1. depletion of ATP and decreased ATP synthesis
  2. mitochondrial damage
  3. influx of intracellular calcium and loss of calcium homeostasis
  4. accumulation of oxygen-derived free radicals (oxidative stress)
  5. defects in membrane permeability/membrane injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what occurs when there is a depletion of ATP and decreased ATP synthesis

A
  1. the plasma membrane NaK ATPase pump fails and Na enters the cell and water follows leading to cell swelling and dilation of the RER
  2. failute of the Ca pump causes excess calcium to enter the cell; that damages a number of systems by increased enzyme activity
  3. if cells switch to glycolysis, glycogen is depleted and lactic acid and inorganic phosphates accumulate which decreases intracellular pH, resulting in decreased activity of some cellular enzymes
  4. as ATP depletion continues, ribosomes detach from the RER leading to decreased protein synthesis
  5. protein misfolding occurs leading to further cell injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what occurs during mitochondrial damage

A
  • cell injury causes formation of the mitochondrial permeability transition that ultimately interferes with mitochonrial oxidative phosphorylation
  • following injury, mitochondria can leak cytochrome c into the cytosol that may trigger apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what occurs when there is an influx of intracellular calcium and loss of calcium homeostasis

A
  • activation of phospholipase A
  • breaks down the normal phospholipids of the inner mitochondrial membrane and other cell membranes
  • generates arachidonic acid (substrate for many lipid mediators of inflammation)
  • activation of proteases that cause cytoskeleton and membrane damage
  • ATPases
  • endonucleases that degrade chromatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what occurs when there is accumulation of oxygen-derived free radicals (oxidative stress)

A
  • free radicals can damage lipids, proteins, and nucleic acids
  • normally free radicals are scavenged, but when there is an excess of production or decreased removal then oxidative stress occurs
  • free radical damage occurs with chemical and radiation injury, ischemia, microbial killing by neutrophils and macrophages, and cellular aging
  • once formed, free radicals damage tissues by: lipid peroxidation of membranes; oxidative modification of proteins; DNA damage
  • cells have multiple mechanisms to remove or neutralize free radicals (antioxidants, iron and copper binding proteins, free radical-scavening enzyme systems)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what occurs during defects in membrane permeability/membrane injury

A
  • cell membranes can be damaged by a variety of insults including (ATP depletion, free radicals, Ca influx, and activation of phospholipases) as well as being directly damaged by infectious agents, complement, killer t cells, and physical and chemical agents
  • membrane damage allows cell contents to leak into the plasma and these can be detected in blood samples (ALT, AST - liver damage)
18
Q

what are the 3 kinds of reversible cell injury

A
  • cell swelling
  • fatty change/lipidosis
  • glycogen accumulation
19
Q

what is cell swelling

reversible cell injury

A
  • increased cell size and volume due to overload of water caused by a failure to regulate the ingress and excretion of water
  • ultrastructural changes (membrane alterations, loss of intercellular junctions, mitochondrial swelling, rarefaction, dialtion of ER, clumping of nuclear chromatin)
20
Q

what is fatty change

reversible cell injury

A
  • accumulation of fat in vacuoles in the cytoplasm of non-adipose cells
  • excessive entry of fatty acids due to excessibe dietary intake or increased mobilization
  • excessive fatty acid synthesis and triglyceride formation due to excessive intake of carbs
  • decreased oxidation of fatty acids due to hepatocyte dysfunction
  • decreased apoprotein synthesis with decreased export of lipoproteins
  • impaired scretion of lipoproteins
  • ex: hepatic lipidosis -> accumulation of fat in hepatocytes -> the liver is enlarged, swollen, yellow and friable
21
Q

what is glycogen accumulation

reversible cell injury

A

occurs in the liver associated with stess or increased levels of steroids and does not lead to cell death

22
Q

what is the significance and fate of acute cell swelling

A
  • if adequate oxygen is restored to the cells and membrane injury is repaired before a certain point is reached, most cells can be restored to normal or nearly normal function
  • some cells may retain evidence or previous injury in the form of lipofuscin accumulation after autophagocytosis of damaged organelles
  • after the point of no return -> irreversitble cell injury -> cell death
23
Q

what is necrosis

A
  • the spectrum or morphologic changes (gross, histologic, and ultrastructural) that follow cell death in a living tissue
  • cell swells
  • plasma mebrane rupute
  • cellular and nuclear lysis causes inflammation
24
Q

what is apoptosis

A
  • one group of pathways of cell death that are the result of a regulated intracellular program that activates intracellular enzymes to cause degradation of cell proteins and DNA, cell shrinkage, and death
  • formation of blebbing
  • cell breaks apart into several apoptotic bodies, which are then phagocytosed
  • no inflammation
25
Q

cytoplasm of necrosis in a cell

A
  • hypereosinophilic due to loss of RNA in the cytoplasm and DNA stain with the blue dye and denatured cytoplasmic proteins
  • calcification of cells
  • membrane disruption, dilated mitochonria w/ large amorphous densities, and cytoplasmic myelin figures
26
Q

nucleus of necrosis cell

what is pyknosis

A

nuclear shrinkage and increased basophilic

27
Q

nucleus of necrosis cell

what is karyorrhexis

A

nucleus fragments (usually following pyknosis)

28
Q

nucleus of necrosis cell

what is karyolysis

A

fading or disappearance of the nucleus

29
Q

patterns of necrosis

multifocal random

A

usually infectious casuses

30
Q

patterns of necrosis

massive

A

usually toxic or nutritional causes

31
Q

patterns of necrosis

zonal or regional

A

usually toxic, hypoxic, or metabolic causes

32
Q

what is coagulative necrosis

A
  • ischemia or toxins
  • for a few days the cells maintain their basic outline
  • eventually enzymatic action and entering leukocytes leads to proteolysis and loss of the cell outline
  • ischemic necrosis of an extremity with subsequent coagulation necrosis is called dry gangrene
  • when the action of bacteria causes liquefaction of the gangrenous tissue it is called wet gangrene
33
Q

what is liquefactive necrosis

A
  • bacterial, fungal, or lytic viral infections and cells are digested by their own enzymes, bacterial toxins, or the enzymes of leukocytes
  • cells are replaced by neutrophils and macrophages
  • focal collections of WBCs (pus) and cellular debris are termed abscesses
  • cell outline lost
34
Q

what is fat necrosis

A

enzymatic descruction of fat with mineralization

35
Q

what is caseous necrosis

A

cheese like gross appearance of coagulation necrosis with subsequent inflammation and sometimes calcification that occurs with some bacteria

36
Q

what is the morphology of apoptosis

A
  • cell shrinkage
  • chromatin condensation
  • cytoplasmic blebs and apoptotic bodies
  • phagocytosis of apoptotic cells or bodies
37
Q

what are the causes of apoptosis

A
  • radiation, toxins, free radials causing DNA damage
  • withdrawal of growth factors or hormones
  • receptor ligand interactions
  • cytotoxic T lymphocytes
  • DNA damage
38
Q

what are the 3 mechanisms of apoptosis in pathologic conditions

A
  1. initiation phase (extrinsic or intrinsic pathway - caspases become catalytically active)
  2. execution phase (caspases cleave cytoskeletal and nuclear membrane proteins, activate DNAases that induces internucleosomal cleavage of DNA)
  3. removal of dead cells (dying cells attract phagocytes by molecular markers on their surface, macrophages remove dead cells w/o causing inflammation)
39
Q

what is postmortem autolysis

A
  • leads to softening and friability of tissues grossly
  • may be difficult to distinguish from necrosis histologically
  • involves entire tissue
  • no associated inflammatory response
  • RBC in adjacent blood vessels are also autolyzed
40
Q

what are some examples of changes that occur after death in an organism

A
  • rigor mortis
  • algor mortis
  • livor mortic
  • postmortem blood clot
  • hemoglobin imbition
  • bile imbition
  • pseudomelanosis
  • bloating
41
Q

cell injury

oxygen and energy deprivation

A
  • hypoxia and anoxia
  • ischemia or infarction
  • decreased oxygen carrying capacity
  • decreased oxygenation of the blood
  • blockage of cellular respiration
42
Q

what is autolysis

A

degradation of a cell by its own enzymes after it has died

Foundational toolkit III - wk1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions