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Pathophys Test 1 > JG Day 1- Altered Cellular Biology > Flashcards

JG Day 1- Altered Cellular Biology Flashcards

1
Q

What is normal homeostasis?

A

normal internal equilibrium

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2
Q

What is stress (insult) to a cell?

A

Any stimulus that upsets normal homeostasis

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3
Q

What is compensation?

A

body’s attempt to maintain normal homeostasis under stress

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4
Q

What is cell injury?

A

result of stimulus in excess of a cell’s immediate adaptive response (i.e. frostbite)

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5
Q

What is a reversible cell injury?

A

injury which does not kill the cell (anything that doesn’t kill me, makes me stronger)

  • cell will adapt in order to be able to handle stressor
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6
Q

What is irreversible cell injury

A

injury that results in cell death

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7
Q

What is apopsosis?

A

clean, controlled cell death

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8
Q

What is necrosis?

A

Messy, uncontrolled cell death

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9
Q

What is cellular adaptation

A

compensations that occurs on the cellular level

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10
Q

What is atrophy?

A

decrease in size of the cells

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11
Q

What is hypertrophy

A

increase in the size of cells (troph= eating hypertrophy= overeating)

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12
Q

What is hyperplasia?

A

Increase in number of cells

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13
Q

What is metaplasia?

A

Chnage of cell from one type to another- can be normal or abnormal

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14
Q

What is dysplasia?

A
  • Abnormal cells that are not necessarily cancer
    • not Cancer yet but is a big step
  • dysplastic cells are NEVER normal cells. there should not be any dysplastic tissue in your body.
    • cells reproducing out of control
  • example dysplasia= wart
  • Less reversible
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15
Q

What is neoplasia?

A

Abnormal disorganized growth, also known as a tumor= can be cancer

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16
Q

Which cells in your body are not mitotic (do not have the ability to divide)?

A
  • Brain
  • Heart- do have stem cells but ver low rate
  • Skeletal

Heart and skeletal grow by hypertrophy

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17
Q

What type of change would occur when ciliated pseudostratified columnar epithelial changes to stratified squamous cells in the bronchi?

A

Metaplastic change

  • This is a compensation to the chronic insulin of smokers
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18
Q

What are come common themes in cell injury?

A
  • ATP depletion
  • Free radicals and reactive oxygen species
  • increase in intracellular Ca
  • Defects in plasma membrane
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19
Q

What happens with the ATP depletion in cell injury?

A
  • Oxygen deficiency greatly decreases ATP production
  • lack of ATP prevents function of Na/K ATPase
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20
Q

What are free radicals and ROS roll in cellular injury?

A
  • Cause oxidation of membrane and other structures
  • particularly problematic with reperfusion
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21
Q

What is a free radical?

A

Atom/molecule that has an unpaired electron (in outer orbit)

  • highly reactive
    • steal electron from weaker and weaker molecules
  • wants to “grab” an electron from another molecule (this in turn will then make that molecule a free radical)
    • If the free radical steals the electron from protein/FFA then that protein/FFA is corrupted
  • We have pathways that stop free radicals
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22
Q

What is a ROS?

A

Reactive oxygen speices that is not a free radical (H2O2)

  • highly reactive molecule that contains oxygen
  • extremely reactive with anything it comes in contact with
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23
Q

Do you have hydrogen peroxide inside body?

A

Only specific immune cells inside body produce hydrogen peroxide in order to kill bacteria

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24
Q

What happens during reperfusion?

A

More oxidative damage

  • The mitochondria and area around it is the most susceptible to damage
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25
Q

What happens to ROS during exercise?

A
  • As you start running, increasing metabolism, ROS increases
  • Oxidative damage increases
  • However, also increase the pathway that stop reactive pathways species (ROS)
  • When you stop running, ROS decreses, but the pathways stopping free radicals stay elevated
    • so, when exercising regularly, oxidative damage level is significantly lower at baseline compared to non exercisers.
      • During excercise, however, oxidative damage increases
26
Q

What is calciums role in cell injury?

A
  • Low ATP and Na gradient prevent removal of Ca and release of Ca from mitochondria and ER
    • Ca takes a lot of energy to pump back out
      • normally, Ca into cell, does it’s thing and it pumped back out
  • Ca activates many enzymes
  • at very high levels of Ca, signals cell apoptosis
27
Q

How does defect in plasma membrane cause cell injury?

A
  • loss of Na gradient, activation of proteases and phospholipases
    • Na gradient essential for many cell “housekeeping” functions
  • permeable plasma membrane prevents normal cell function
28
Q

What happens inside the cell during ischemia once pH starts to fall?

A
  • Nuclear chormatin clumping (reversible)
  • swelling of lysosomes (reversible)
    • increase release of lysosomal enzymes (hydrolases), causing autodigestion<— IRREVERSIBLE
29
Q

What happens as a result of decrease function of Na pump when ATP is decreased d/t ischemia?

A
  • Increase in intracellular Na
  • Increase in extracellular K
  • Increase intracellular Ca
    • Ca causes cell to be too active
    • also signals apoptosis
  • This all causes increase in H2O
    • Causing acute cellular sweilling
30
Q

What happens to protein production with a decrease in cellular ATP from ischemia?

A
  • Dilation of ER
  • Detachment of ribosomes
  • decrease in protein synthesis<– BIG DEAL
    • therefore, cell can’t repair damage to the cytoskeleton
  • lipid deposition
    • membrane damage
31
Q

What happens to cell contents after cell membrane damage?

A
  • Loss of phosphoplipids, alteration cytoskseleton, activation of infalmmation, increase free radicals, lipid breakdown
  • release of enzymes (I.E. CPK, LDH)
  • Increase Ca influx
  • increase Ca in mitochondria
32
Q

What are some cell characteristics observed in reversible cell injury?

A
  • Blebs in plasma membrane but still intract
  • ribosomes detach from rough ER
  • Mitrochondria swells
  • lysosomes digest organelles that aren’t working
  • clumping DNA
  • cell will adapt to deal with stressor
33
Q

What are cell characteristics observered in irreversible cell injury?

A
  • defects in plasma membran e(game over)
  • ER falls apart
  • Rupture lysosomes and autolysis (autodigestion)
  • DNA clumps
    • karyolysis- cutting up DNA

Bolded 3 most important. Once cell has those occuring, cell is gone

34
Q

Definition hypoxia?

A

low tissues oxygen level

35
Q

What is definition of anoxia?

A
  • very low tissue oxygen level, no oxygen
36
Q

Definition of hypoxemia?

A
  • Low blood oxygen tension (decrease o2 sat)
  • low oxygen in BLOOD (as opposed to hypoxia= low tissue oxygen)
  • Hypoxemia will lead to hypoxia
37
Q

What can cause hypoxia without hypoxemia?

A

anemia

38
Q

What can cause hypoxemia without hypoxia?

A

polycythemia

39
Q

What happens to rate of free radical production after time of ischemia

A

Increase significantly due to time making up for the ATP that could not be produced during ischemia

  • This high rate of production of free radicals overwhelms system that neutralizes free radicals, and you get oxidative damage
40
Q

How can you identify if a molecule has a free radical?

A

Dot by the structure

41
Q

What is SOD?

A

Superoxide dismutase

  • converts superoxide to h2o2 (hydrogen peroxide)
  • huge benefit because superoxide anion is extremely reactive
    • SOD is mechanism for controlling free radicals
42
Q

What is catalase?

A
  • What cells use to convert H2O2 (which is an ROS) to H2O
43
Q

What is glutathione?

A
  • converts OH (hydroxyl radicals)–> H2O
  • In liver, detoxifies acetaminophen
    • in overodse, acetaminophen uses up stockpile of glutathione
    • acetylcysteine given during overdose to increase cysteine available for resynthesis of glutathrione
44
Q

What is apoptosis?

A
  • Clean, controlled cell death
  • cell goes into self destruct mode
    • nuclear chromatin condensation and fragmentation
    • cytoplasmic budding and phagocytosis of the extruded apoptotic bodies
  • phagocyte eats apoptotic bodies from cell
  • cytoplasm never ends up in ECF
    • DOES NOT trigger any inflammation response from body
45
Q

What is the differnece in body response in necrotic cell death vs apoptotic cell death

A
  • In necrotic cell death, contents of cell end up in ECF and trigger immune system to start repair process (causes inflammation response)
46
Q

What is coagulative necrosis?

A
  • what happens most of time in body when tissue dies
  • loss of nuclei and clumping of cytoplasm but preservation of basic outlines of cells
47
Q

What is liquefactive necrosis?

A
  • immune cells preventing fungus from growing and whatever tissue where fungus was is destroyed.
  • From book “, in contrast to coagulative necrosis, is characterized by digestion of the dead cells, resulting in transformation of the tissue into a liquid viscous mass.”
  • common in brain tissue after ischemic stroke
48
Q

What is caseous necrosis?

A
  • often happens in TB
  • TB cells deposit lipoproteins that has a yellow-whie and cheesy appearance
49
Q

What is fat necrosis?

A
  • focal area of fat destruction/saponification
  • occurs during pancreatitis, causing saponification in the mesentery
    • calcium bounds up to the fat that is being digested, causing plasma calcium levels to fall
50
Q

What is gangrenous necrosis?

A
  • Circulation bad and blood can’t get there to fight the infection
  • types
    • dry gangrene
    • wet gangrene- typically affects internal organs, bedsores
    • gas gangrene- bacterial infection of clostridium perfringens
51
Q

What is a telomere? Telomerase?

A
  • form end of chromosome
    • analogous to end of shoelace to protect damage
  • when telomeres shorten, then cell can’t replicate again
  • each cell has a certain amount of telomerase activity which can lengthen the telomere everytime it replicates
    • high telomerase activity in germ/stem cells (indefinite amoutn telomerase in germ cells, slowly declining in stem cells)
    • limited telomerase activity in normal cells
  • Cancer cells “turn off the telomeric clock” and allows them to replicate and allows tumor cell immortalization
52
Q

Why is plasma Ca level a horrible indication of Calcium status?

A

because Ca is in your bones

  • only free Calcium has effect on body
  • Calcium binds to albumin, so when albumin is affected, Ca is affected
53
Q

What happens if calcium and phosphorus are both high?

A

Ca and Phos will preceipitate out of body

54
Q

What do ALT and AST test for?

A
  • Hepatocyte necrosis
55
Q

What does alkaline phosphatase and gamma-GT test for?

A

biliary duct issues

56
Q

What is a possible problem when bilirubin is elevated?

A

usually liver problem

57
Q

What makes albumin?

A

Liver

58
Q

What is happening if LDH is high?

A

some cells, somewhere is dying. non specfiic

59
Q

What are reticulocytes?

A

baby RBC

  • Only 1% RBC are reticulocytes. Only reticulocytes for one day
  • indication for how fast bone marrow is making RBC right now
60
Q

What is hemogloin? hematocrit? relationship?

A
  • Hemoglobin- how much protein in blood
  • hematocrit- volume made of RBC
  • HCT should be about 3 times Hgb
61
Q

What is mean corpuscular volume?

A

average size rbc

62
Q

What does INR indicate?

A

how fast you clot compared to a normal person

Pathophys Test 1 (7 decks)

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