JG Day 1- Altered Cellular Biology Flashcards

(62 cards)

1
Q

What is normal homeostasis?

A

normal internal equilibrium

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

What is stress (insult) to a cell?

A

Any stimulus that upsets normal homeostasis

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

What is compensation?

A

body’s attempt to maintain normal homeostasis under stress

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

What is cell injury?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is irreversible cell injury

A

injury that results in cell death

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

What is apopsosis?

A

clean, controlled cell death

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

What is necrosis?

A

Messy, uncontrolled cell death

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

What is cellular adaptation

A

compensations that occurs on the cellular level

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

What is atrophy?

A

decrease in size of the cells

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

What is hypertrophy

A

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

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

What is hyperplasia?

A

Increase in number of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is metaplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is neoplasia?

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are free radicals and ROS roll in cellular injury?

A
  • Cause oxidation of membrane and other structures
  • particularly problematic with reperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Do you have hydrogen peroxide inside body?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens during reperfusion?

A

More oxidative damage

  • The mitochondria and area around it is the most susceptible to damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What happens to ROS during exercise?
* 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
What is calciums role in cell injury?
* 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
How does defect in plasma membrane cause cell injury?
* 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
What happens inside the cell during **ischemia** once pH starts to fall?
* Nuclear chormatin clumping (reversible) * swelling of lysosomes (reversible) * increase release of lysosomal enzymes (hydrolases), causing autodigestion\<--- **IRREVERSIBLE**
29
What happens as a result of decrease function of Na pump when ATP is decreased d/t ischemia?
* 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
What happens to protein production with a decrease in cellular ATP from ischemia?
* 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
What happens to cell contents after cell membrane damage?
* 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
What are some cell characteristics observed in reversible cell injury?
* 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
What are cell characteristics observered in irreversible cell injury?
* **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
Definition hypoxia?
low tissues oxygen level
35
What is definition of anoxia?
* very low tissue oxygen level, no oxygen
36
Definition of hypoxemia?
* Low blood oxygen tension (decrease o2 sat) * low oxygen in BLOOD (as opposed to hypoxia= low tissue oxygen) * Hypoxemia will lead to hypoxia
37
What can cause hypoxia without hypoxemia?
anemia
38
What can cause hypoxemia without hypoxia?
polycythemia
39
What happens to rate of free radical production after time of ischemia
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
How can you identify if a molecule has a free radical?
Dot by the structure
41
What is SOD?
Superoxide dismutase * converts superoxide to h2o2 (hydrogen peroxide) * huge benefit because superoxide anion is extremely reactive * SOD is mechanism for controlling free radicals
42
What is catalase?
* What cells use to convert H2O2 (which is an ROS) to H2O
43
What is glutathione?
* 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
What is apoptosis?
* 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
What is the differnece in body response in necrotic cell death vs apoptotic cell death
* In necrotic cell death, contents of cell end up in ECF and trigger immune system to start repair process (causes inflammation response)
46
What is coagulative necrosis?
* 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
What is liquefactive necrosis?
* 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
What is caseous necrosis?
* often happens in TB * TB cells deposit lipoproteins that has a yellow-whie and cheesy appearance
49
What is fat necrosis?
* 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
What is gangrenous necrosis?
* 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
What is a telomere? Telomerase?
* 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
Why is plasma Ca level a horrible indication of Calcium status?
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
What happens if calcium and phosphorus are both high?
Ca and Phos will preceipitate out of body
54
What do ALT and AST test for?
* Hepatocyte necrosis
55
What does alkaline phosphatase and gamma-GT test for?
biliary duct issues
56
What is a possible problem when bilirubin is elevated?
usually liver problem
57
What makes albumin?
Liver
58
What is happening if LDH is high?
some cells, somewhere is dying. non specfiic
59
What are reticulocytes?
baby RBC * Only 1% RBC are reticulocytes. Only reticulocytes for one day * indication for how fast bone marrow is making RBC right now
60
What is hemogloin? hematocrit? relationship?
* Hemoglobin- how much protein in blood * hematocrit- volume made of RBC * HCT should be about 3 times Hgb
61
What is mean corpuscular volume?
average size rbc
62
What does INR indicate?
how fast you clot compared to a normal person