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intro + cell injury Flashcards

lect 1 & 2

1
Q

what is the main cause of death in developed country?

A

cancer and cardiovascular disease

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2
Q

what is the main cause of death in underdeveloped countries?

A

infectious disease

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3
Q

what is 1 DALY?

A

1 disability-adjusted life year = loss of one year of full health

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4
Q

which killers have increased since 1990?

A

high blood pressure, smoking, obesity, alcohol consumption, ambient pollution

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5
Q

which killers have decreased since 1990?

A

child starvation, house-air pollution

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6
Q

is genetic or environment more important for determining disease?

A

environment (lifestyle)

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7
Q

what is the difference between symptoms and signs

A

symptoms = phenomenon you experience
signs = visible manifestation; observable phenomenon

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8
Q

what is a sequel?

A

occurs with time; direct outcome of something (ex skin lesion sequel is a scar)

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9
Q

how are biopsy tissues fixed?

A

with formaldehyde, embedded with paraffin, sliced and stained

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10
Q

what is the best way to get a biopsy? why?

A

endoscopy in respiratory, gastrointestinal, reproductive system; does not require surgery

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11
Q

what is histopathology?

A

microscopic examination of tissue in order to study the manifestation of disease

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12
Q

what is cytology?

A

looking at individual cells

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13
Q

what are characteristics of epithelial tissue?

A

protective, secretory, involved in absorption, contractile, made of collagen, fibroblasts

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14
Q

what are the 5 methods of adaptation to cellular stress?

A

hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia

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15
Q

what are the causes of atrophy?

A

decrease workload, loss of innervation, inadequate blood supply, hormonal stimulation, nutrient supply

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16
Q

what are the causes for hypertrophy?

A

increased workload, hormonal treatment, pathological hypertrophy

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17
Q

what is enzyme induction

A

variant of hypertrophy in smooth endoplasmic reticulum of hepatocytes (liver). increases levels of enzymes

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18
Q

what is metaplasia? where does it often happen?

A

substituting a cell type with another.
in the lungs (mucociliary transport system)

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19
Q

what are dysplastic cells?

A

non-normal cells of non identical size and shape

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20
Q

what is anaplasia?

A

progression of dysplasia due to genetic mutations leading to camcer

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21
Q

when does cell damage become irreversible?

A

when the cell’s ultrastructure changes (although there is No distinct indicator of the boundary between reversible and lethal injury)

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22
Q

what are the 4 target areas of cell injury?

A

mitochondria
plasma membrane
endoplasmic reticulum
nucleus

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23
Q

what are the main cellular consequences of cellular damage

A

increased free calcium inside the cell, disruption of lysosomes, release of reactive oxygen species, interruption of protein synthesis, cytoskeleton damage

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24
Q

what is the consequence of mitochondrial damage

A

decreased ATP production through decreased ion pump function at the plasma membrane and decreased oxidative phosphorylation.

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25
Q

what organ is the most vulnerable?

A

brain

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26
Q

what is ischemia

A

inadequate blood supply resulting in inadequate oxygen and nutrients supply

27
Q

what cell types are the most vulnerable to ischemia?

A

neurons

28
Q

5 causes of ischemia?

A

thrombus, embolus, pressure, plaque, spasm

29
Q

what causes impaired erythrocytes?

A

anemia or CO poisoning

30
Q

what is anemia

A

lack of red blood cells

31
Q

5 causes of physical injury

A

mechanical, thermal, altered pressure, radiation, electrical injury

32
Q

what is the most common cause of death by injury around the globe?

A

road traffic deaths

33
Q

what are the 3 types of microorganisms causing infectious diseases

A

viruses, bacteria, parasites

34
Q

how do bacterial toxins disrupt cell function?

A

damage to plasma membrane, cytoskeleton, mitochondria;
disruption in protein synthesis, cell cycle, signal transduction, cell-cell adhesion, vesicular trafficking, exocytosis

35
Q

what activates cell mediated death?

A

infection of cell by a virus. prevents virus replication

36
Q

what is albinism

A

genetic abnormality that affects melanin synthesis

37
Q

what does NA+/K+ pump does?

A

pump 3 NA+ out the cell
pump 2 K+ into the cell

38
Q

how does the cell respond to hypoxic injury?

A

acidification due to glycolysis (break down glycogen, produce lactic acid, decrease cell pH)

39
Q

what are the steps of hypoxic injury?

A
  1. mitochondria swells -> ER dilates -> ribosomes detach (impaired protein synthesis) -> decreased oxidative phosphorylation
40
Q

what causes increased calcium entry during hypoxic injury?

A

plasma membrane breaks: Calcium enters cytosol from mitochondria and outside of cell

41
Q

what does increased calcium do?

A

increases lipid degradation and cytoskeletal damage?

42
Q

definition of a free radical?

A

molecule with an unpaired electron in its outer orbital.
highly unstable; initiates rapid damage

43
Q

what are free radicals in the body called? give examples

A

reactive oxygen species ROS;
superoxide, hydroxyl radical, peroxide

44
Q

what immune cells are specialized to form free radicals?

A

neutrophils and macrophages form ROS in lysosomal bags to kill bacteria.

45
Q

through what processes do free radical injury damage plasma and organelles membrane?

A

lipid peroxidation, protein modifications, DNA damage

46
Q

what organelle produces free radicals?

A

mitochondria. also removes them

47
Q

what 2 enzymes can deactivate free radicals?

A

superoxide dismutase and catalases

48
Q

what is coagulation vs liquefactive necrosis? what is in between both?

A

coagulation = tissue hardens and dead cell retains its outline
liquafactive = tissue turns liquid by enzyme action
combination = caseous necrosis

49
Q

what does caseous necrosis indicate?

A

tuberculosis

50
Q

what is gangrene?

A

ischemic necrosis followed by bacterial infection

51
Q

what leads to apoptosis (programmed cell death)?

A

imbalance between pro and anti-apoptotic proteins

52
Q

4 phenomenon involving apoptosis

A

healthy = embryogenesis and cell turnover
bad = viral infections, neurodegenerative disease

53
Q

what molecules activates caspases and triggers apoptosis?

A

cytochrome C

54
Q

explain the intrinsic pathway for apoptosis initiation

A

mitochondria sense loss of GF/survival signals, increase of pro-apoptotic proteins, DNA damage, misfolded proteins, and initiates apoptosis; involves cytochrome C!!!

55
Q

explain the extrinsic pathway for apoptosis initiation

A

FasL bind Fas or type 1 TNF receptor -> activation of death receptors -> activation of caspases

56
Q

what are Fas ligand and TNFR! receptors linked to?

A

death domains on intracellular side

57
Q

what can block apoptosis?

A

NF-kB

58
Q

what molecule causes the breakdown of the cytoskeleton and fragmentation of the nucleus

A

caspases (involved in apoptosis)

59
Q

in what types of disease is apoptosis absent?

A

cancer or autoimmune disease

60
Q

what causes necrosis vs apoptosis?

A

necrosis is caused by hypoxia/ischemia and ROS;
apoptosis is triggered by radiation, mutations, cell stress

61
Q

different types of intracellular accumulations

A

abnormal metabolism,
defect in protein folding and transport,
lack of an enzyme,
ingestion of indigestible materials,

62
Q

name an example of abnormal metabolism

A

alcohol liver disease: accumulation of fat in the liver cells

63
Q

name examples of indigestible materials

A

silica, coal, tattoos, lipofuscin, melanin, calcium

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