Cells

Question 0

The body’s attempt to maintain normal homeostasis under stress?

• Ex: shivering
• Body temperature decrease by 2 or 3 degrees will cause the body to react, cells will not work anymore. 3 degree increase in temperature and your body’s cells will work, but they will be working faster.

Answer 0

Compensation

Question 1

1) Normal internal equilibrium (pH7.4)?

2) Stimulus which upsets normal homeostasis?

Answer 1

1) Normal Homeostasis

2) Stress (Insult)

Question 2

Result of a stimulus in excess of a cell’s immediate adaptive response?
*Ex: cut off circulation to the arm&raquo_space; cells will start to become injured

Answer 2

Cell injury

Question 3

Injury which does not kill the cell (anything which doesn’t kill me makes me stronger)?
Cells will adapt to whatever insult they have recently experienced in case it happens again = Ex: exercise
This works at the cell level, does not work at the tissue level
Ex: Heart attack - the heart survives but the cells that die are dead. Cells that are dead are dead and they will be replaced by scar tissue.
*At the cell level anything that doesn’t kill me makes me stronger, at the tissue level not necessarily true.

Answer 3

Reversible Cell Injury

Question 4

1) Injury that results in cell death?

2) There are 2 types of cell death, what are they?

Answer 4

1) Irreversible Cell Injury/Cell Death

2) Apoptosis & Necrosis

Question 5

1) Clean controlled cell death?

2) Messy uncontrolled cell death?

Answer 5

1) Apoptosis

2) Necrosis

Question 6

Compensation that occurs on the cellular level?

Answer 6

Cellular Adaptation

Question 7

1) Decrease in the size of cells?
2) Increase in the size of cells?
* This affects (2)??

Answer 7

1) Atrophy
2) Hypertrophy
* Skeletal & Cardiac muscles

Question 8

Increase in number of cells?

Answer 8

Hyperplasia
*Pretty much every other organ will undergo hyperplasia (not the brain)
Ex: BPH - benign prostatic hyperplasia

Question 9

Change of cell from one type to another - can be normal or abnormal?
*This is often a normal occurrence because whatever cell type you had there, it doesn’t feel like it is sufficient to deal with whatever the threat is. Ex: stomach regurgitation, burning away at the lower esophagus

Answer 9

Metaplasia

Question 10

Abnormal cells that are not necessarily cancer?

*Conversion to an abnormal cell type. A cell type that would not occur anywhere in the body.

Answer 10

Dysplasia

Question 11

Abnormal disorganized growth, also known as a tumor - can be cancer?
Ex: wart
This is not necessarily cancer, but it can be cancer.

Answer 11

Neoplasia

Question 12

*So cancers will be ___, cancers will be ___.

Answer 12

Dysplasias
Neoplasias
*but not all dysplastic tissue and not all neoplasias are cancerous

Question 13

An organ that gets bigger will either get bigger by ___ or by ___.

Answer 13

Hypertrophy

Hyperplasia

Question 14

___ of cardiac muscle in response to valve disease (ex: aortic stenosis).

Answer 14

Hypertrophy

Question 15

Reversible changes in cells lining the bronchi:
1) Normal ___ ___
2) Chronic injury or irritation?
Ex: Converting into stratified squamous, this will occur in smokers.The smoke is such an insult that the lung lining needs to become tougher. This is reversible if smoking cessation. Tissue would return to normal.
3) Persistent severe injury or irritation? (on its way to becoming cancer)

Answer 15

1) Normal Ciliated Epithelium
2) Metaplasia
3) Dysplasia

Question 16

If we kill cells then they die. Fortunately for most of the body we can replace dead cells - except for the ___ & ___.

Answer 16

Heart & Brain (neurons)

Question 17

Common Themes in Cell Injury:

1) ___ depletion
2) ___ & ___
3) Increase in ____
4) Defects in ___

Answer 17

1) ATP depletion
2) Free Radicals & Reactive Oxygen Species (ROS)
3) Increase in Intracellular Calcium
4) Defects in Plasma Membrane

Question 18

Common Themes in Cell Injury:

Oxygen deficiency greatly decreases ATP production, lack of ATP prevents function of Na/K ATPase, etc. This is the biggest common theme?

Answer 18

ATP depletion

Question 19

Common Themes in Cell Injury:

These cause oxidation of membranes and other structures and are particularly problematic with reperfusion?

Answer 19

Free Radicals & Reactive Oxygen Species (ROS)

Question 20

___ also produces ROS (very reactive, typically oxidize whatever they come in contact with). Many of the ROS are known as free radicals.
~These are really big problems with ___. Someone has a heart attack - thromboembolic event blocking some artery - have to restore blood flow but when we restore blood flow we are going to have oxidative damage as a result.

Answer 20

Oxygen

Re-perfusion

Question 21

Common Themes in Cell Injury: Increase in Intracellular Calcium

1) Low ___ & ___ gradient prevent removal of calcium &
2) Release of calcium from ___ & ___
3) Calcium activates many ___
4) At very high levels, calcium signals ___

Answer 21

1) Low ATP & sodium gradient
2) Mitochondria & ER
3) Enzymes
4) Apoptosis

Question 22

~When a little bit of calcium comes into the cell that is a signal for the cell ???
~BUT when A LOT of calcium comes into the cell it is a signal for the cell to ___!
~Get calcium out of the cell by the sodium-calcium exchanger (sodium comes in and calcium comes out), to get the really steep gradient use the ATP-Calcium pump. If we are running low on ATP, both of these mechanisms will fail and cell will die from too much calcium inside the cell.

Answer 22

To do what it does best

Die

Question 23

Common Themes in Cell Injury: Defects in Plasma Membrane

1) This occurs as a result of loss of ___ gradient, activation of ___ and ___.
2) ___ ___ ___ prevents normal cell function.

Answer 23

1) sodium gradient
proteases
phospholipases
2) Permeable plasma membrane

Question 24

Reversible Cell Injury:

1) This ___ is not damaged yet so if we can restore the oxygen, restore the ATP production, the cell can recover from this.
* The ___ will swell, cutting protein production, but again if we can start getting ___ ___ back up can start making proteins again.
* ___ has ___ but it is still intact.

Answer 24

1) Membrane
2) Rough Endoplasmic Reticulum
ATP production
3) DNA has clumped

Question 25

Irreversible Cell Injury:

1) ___ ___ = Defects in the membrane > releases lysosomal enzymes.
2) ___ is not just clumped now it actually starts breaking it up.
* ___ = chopping up the nucleus
* Once we chop up the DNA its game over. Once the cell loses its DNA there is no point in recovering because we can’t make proteins anymore.

Answer 25

1) Membrane damage
2) DNA
* Karyolysis

Question 26

1) Low tissue oxygen level?

2) Very low tissue oxygen level, no oxygen (way worse)?

Answer 26

1) Hypoxia

2) Anoxia

Question 27

1) Low blood oxygen tension (decreased oxygen saturation)?
2) Insufficient blood supply to tissue or organ?
3) Ischemia with necrosis?
4) Restoration of blood supply that had been cut off?

Answer 27

1) Hypoxemia
2) Ischemia
3) Infarction
4) Reperfusion

Question 28

1) Embolus would result in ___.
2) Anemia can also cause ___, patients with anemia can still have a normal O2 saturation though (not necessarily ___). Can have someone with anemia who has ___ and they do not have ___.

Answer 28

1) Hypoxemia
2) Hypoxia
Hypoxemic
Hypoxia
Hypoxemia

Question 29

When we restore blood flow and now have fully oxygenated RBCs coming in, unfortunately we produce lots of ___.

Answer 29

Reactive Oxygen Species (ROS)

Question 30

A ___ is a molecule that has an unpaired electron (extra electron).

Answer 30

Free radical

Question 31

Our 3 big antioxidants are?

Answer 31

Superoxide dismutase (SOD)
Catalase
Glutathione

Question 32

___ is going to grab the superoxide anion and convert it into a hydrogen peroxide. (O2 + H2O = H2O2)

Answer 32

Superoxide dismutase (SOD)

Question 33

___ is usually the enzyme that we use to make H2O2 in mitochondria when we need to kill bacteria. Well this enzyme most every place else goes the opposite direction. We thus convert hydrogen peroxide to water using ___.

Answer 33

Catalase

Catalase

Question 34

We can also use ___ to convert hydrogen peroxide to a hydroxyl radical which we then can convert back to water.

Answer 34

Glutathione

Question 35

****3 major antioxidants - SOD, Catalase and Glutathione

These will be elevated with ___ - it will increase ROS and thus antioxidants will be increased in this person.

Answer 35

Exercise

Question 36

In Apoptosis the initial changes consist of ___ ___ ___ & ___, followed by ___ ___ & ___ of the extruded apoptotic bodies.

Answer 36

Nuclear chromatin condensation
Fragmentation
Cytoplasmic budding
Phagocytosis

Question 37

Signs of Coagulation Necrosis include ___ ___, ___ ___ & eventual ___ ___.

Answer 37

Chromatin clumping
Organellar swelling
Membrane damage

Question 38

1) Membrane damage, cell disintegrates, cytoplasmic proteins leak out & inflammation occurs in this process?
2) Cell gets signal to die, nothing leaks out, no inflammation with this process?

Answer 38

1) Necrosis

2) Apoptosis

Question 40

With membrane damage the stuff in the cytoplasm is going to leak out and then the stuff in the extracellular space is going to leak in and the cell will die. And then we will have to send macrophages over to clean up the mess. It turns out that having stuff in the cytoplasm leak out into the extracellular environment is a signal for inflammation. And inflammation is going to be what comes in and cleans up the mess. So this process is going to be very inflammatory, we are going to need to recruit cells to clean up this muck. What is this process?

Answer 40

Necrosis

Question 41

_____: What you get when you have ischemia in most places in your body (in fact every place except for your brain). The structure will be intact but the cells are all dead.
Ex: So if you were to cut off blood flow to the kidney the cells would all die but they would die in place. Everything would look just like where it was but everything is dead. This is what is going to happen with ischemia. Every place except for your brain.

Answer 41

Coagulative Necrosis

Question 42

_____: An example of this would be a fungal abscess in the kidney. Everything in the abscess (kidney structure wise) has been obliterated. There is nothing in here that looks like kidney anymore. The enzymes that are being secreted by the immune cells and quite often by the infection dissolve structures.
*This is also what we get with ischemia in the ___ = neutrophils & macrophages will release digestive enzymes that will basically hollow out wherever the dead spot is. So rather than the tissue all being intact what you will end up with is what looks like an abscess, its a clean abscess, there is no infectious agent in there.

Answer 42

Liquefactive Necrosis

*Brain

Question 43

Types of Necrosis:

1) Kidney infarct exhibiting ___ NECROSIS with loss of ___ & clumping of the ___ but with preservation of basic outlines of glomerular & tubular architecture.
2) ___ NECROSIS in the kidney caused by fungal seeding. The focus is filled with white cells & cellular debris, creating a ___ ___ that obliterates the normal architecture.

Answer 43

1) Coagulative Necrosis
nuclei
cytoplasm
2) Liquefactive Necrosis
renal abscess

Question 44

1) ___ ___ = infections, abscesses & ischemia in the BRAIN

2) ___ ___ = This occurs everywhere else with ischemia except for the brain

Answer 44

1) Liquefactive Necrosis

2) Coagulative Necrosis

Question 45

Types of Necrosis:

1) This is what is produced by Tuberculosis (the debris is yellow-white & cheesy - waxy stuff)?
2) Lets say you have acute pancreatitis and pancreatic enzymes break out of the pancreas and start digesting the fat in the greater omentum or lesser omentum. What is going to happen? They are going to digest this fat and we are going to end up with ??? It is basically going to turn your abdominal fat into soap.

Answer 45

1) Caseous Necrosis

2) Fat Necrosis

Question 46

Fat Necrosis & Acute Pancreatitis:
What happens to calcium levels in people who have acute necrosis (high, low or normal)? Initially ___ increases the chance of acute pancreatitis. But once acute pancreatitis occurs calcium levels ___.

Answer 46

-High calcium levels
-Decrease
(because all of this fat being turned into soap, it binds up calcium)

Question 47

Types of Gangrene:

1) This type usually seen with diabetics & frost bite?
2) Typically affects internal organs; bowel as well as bed sores?
3) Involves bacterial infections of clostridium perfringens?

Answer 47

1) Dry Gangrene
2) Wet Gangrene
3) Gas Gangrene

Question 48

___ are the ends of chromosomes. They don’t really code for anything important but they are important. So their a 6 nucleotide repeat, that just repeats, and repeats and repeats. Here is the problem - every time a cell divides, the ___ get a little bit shorter. When they are all gone, the cell can’t divide anymore. At some point it reaches ___ ___ (can’t replicate anymore). It doesn’t die it just can’t replicate anymore.

Answer 48

Telomeres
Telomeres
Replicative Senescence

Question 49

Telomeres = This is a great protection against cancer. The cancer actually has to turn on an enzyme called ___ - this actually lengthens this every-time it replicates. Which means one more thing cancer has to do in order to be successful.

Answer 49

Telomerase

Question 50

We actually have to lengthen the telomere on our ___ ___. So we turn on ___ on ___ ___. For eggs its telomeres will have about 70 replications (telomeres normal length), but sperm actually gets longer the older a man is. Because spermatogonia (every time they divide) the telomere gets longer. An 18 year old boy would have a normal length telomere, but an 80 year old man would have an extra long telomere. So the old mans kids would therefore be likely to live longer. ___ ___ have telomerase turned on to some extent but not completely.

Answer 50

Germ cells
Telomerase
Germ cells
Stem cells

Question 51

*Telomere-telomerase hypothesis & proliferative capacity:
Telomere length is plotted against the number of ___ ___. In normal ___ ___, there is no telomerase activity, and telomeres progressively shorten with increasing cell divisions until growth arrest or ___ occurs.

Answer 51

• Cell divisions
• somatic cells
• senescence

Question 52

*Telomere-telomerase hypothesis & proliferative capacity:
___ ___ & ___ ___ both contain telomerase activity, but only ___ ___ have sufficient levels of the enzyme to maintain telomere length indefinitely. Telomerase activation in ___ ___ turns off the “telomeric clock” that normally limits the proliferative capacity of somatic cells, resulting in ___ ___ immortalization.

Answer 52

• Germ cells
• Stem cells
• Germ cells
• Cancer cells
• Tumor cell

Question 53

With this process the cell gets the signal to die. So the cell dies by making little apoptotic bodies. The cell breaks up into little pieces. The little apoptotic bodies are still surrounded by plasma membrane. So nothing is leaking out of the cell into the extracellular environment. So this is not going to be inflammatory. Nothing leaks out. If the cell had CK in it and we measured CK we would not see it in the blood test because it didn’t leak. And then some phagocyte > maybe a macrophage, maybe a nearby epithelial cell will eat these little apoptotic bodies (think of them as fun-sized snicker bars). This is what our nearby phagocyte will do > eat these things. Nothing was ever exposed to the outside and it is therefore not inflammatory. What is this process?

Answer 53

Apoptosis