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
what organ is the most vulnerable?
brain
26
what is ischemia
inadequate blood supply resulting in inadequate oxygen and nutrients supply
27
what cell types are the most vulnerable to ischemia?
neurons
28
5 causes of ischemia?
thrombus, embolus, pressure, plaque, spasm
29
what causes impaired erythrocytes?
anemia or CO poisoning
30
what is anemia
lack of red blood cells
31
5 causes of physical injury
mechanical, thermal, altered pressure, radiation, electrical injury
32
what is the most common cause of death by injury around the globe?
road traffic deaths
33
what are the 3 types of microorganisms causing infectious diseases
viruses, bacteria, parasites
34
how do bacterial toxins disrupt cell function?
damage to plasma membrane, cytoskeleton, mitochondria; disruption in protein synthesis, cell cycle, signal transduction, cell-cell adhesion, vesicular trafficking, exocytosis
35
what activates cell mediated death?
infection of cell by a virus. prevents virus replication
36
what is albinism
genetic abnormality that affects melanin synthesis
37
what does NA+/K+ pump does?
pump 3 NA+ out the cell pump 2 K+ into the cell
38
how does the cell respond to hypoxic injury?
acidification due to glycolysis (break down glycogen, produce lactic acid, decrease cell pH)
39
what are the steps of hypoxic injury?
1. mitochondria swells -> ER dilates -> ribosomes detach (impaired protein synthesis) -> decreased oxidative phosphorylation
40
what causes increased calcium entry during hypoxic injury?
plasma membrane breaks: Calcium enters cytosol from mitochondria and outside of cell
41
what does increased calcium do?
increases lipid degradation and cytoskeletal damage?
42
definition of a free radical?
molecule with an unpaired electron in its outer orbital. highly unstable; initiates rapid damage
43
what are free radicals in the body called? give examples
reactive oxygen species ROS; superoxide, hydroxyl radical, peroxide
44
what immune cells are specialized to form free radicals?
neutrophils and macrophages form ROS in lysosomal bags to kill bacteria.
45
through what processes do free radical injury damage plasma and organelles membrane?
lipid peroxidation, protein modifications, DNA damage
46
what organelle produces free radicals?
mitochondria. also removes them
47
what 2 enzymes can deactivate free radicals?
superoxide dismutase and catalases
48
what is coagulation vs liquefactive necrosis? what is in between both?
coagulation = tissue hardens and dead cell retains its outline liquafactive = tissue turns liquid by enzyme action combination = caseous necrosis
49
what does caseous necrosis indicate?
tuberculosis
50
what is gangrene?
ischemic necrosis followed by bacterial infection
51
what leads to apoptosis (programmed cell death)?
imbalance between pro and anti-apoptotic proteins
52
4 phenomenon involving apoptosis
healthy = embryogenesis and cell turnover bad = viral infections, neurodegenerative disease
53
what molecules activates caspases and triggers apoptosis?
cytochrome C
54
explain the intrinsic pathway for apoptosis initiation
mitochondria sense loss of GF/survival signals, increase of pro-apoptotic proteins, DNA damage, misfolded proteins, and initiates apoptosis; involves cytochrome C!!!
55
explain the extrinsic pathway for apoptosis initiation
FasL bind Fas or type 1 TNF receptor -> activation of death receptors -> activation of caspases
56
what are Fas ligand and TNFR! receptors linked to?
death domains on intracellular side
57
what can block apoptosis?
NF-kB
58
what molecule causes the breakdown of the cytoskeleton and fragmentation of the nucleus
caspases (involved in apoptosis)
59
in what types of disease is apoptosis absent?
cancer or autoimmune disease
60
what causes necrosis vs apoptosis?
necrosis is caused by hypoxia/ischemia and ROS; apoptosis is triggered by radiation, mutations, cell stress
61
different types of intracellular accumulations
abnormal metabolism, defect in protein folding and transport, lack of an enzyme, ingestion of indigestible materials,
62
name an example of abnormal metabolism
alcohol liver disease: accumulation of fat in the liver cells
63
name examples of indigestible materials
silica, coal, tattoos, lipofuscin, melanin, calcium