Altered Cell Biology Flashcards
0
Q
Almost all the compensation that is going to occur in the body is going to happen at what level?
A
The cellular level
1
Q
When does compensation become counterproductive?
A
In a lot of disease states.
2
Q
Increase in the size, not the number is?
A
Hypertrophy.
3
Q
Where do we see hypertrophy? Why don’t we see hyperplasia here?
A
Heart, brain and Skeletal Muscle. We don’t see hyperplasia because we don’t get more cells in these areas.
4
Q
Increase in cell number, all the same size?
A
Hyperplasia
5
Q
One normal epithelial cell converting to another normal epithelial cell type is termed?
A
Metaplasia
6
Q
Is the resulting normal cell type in metaplasia normal for that area? Name an example.
A
No. Smoking-the normal columnar epithelial cells of the bronchi and bronchioles will convert to stratified squamous even though it is not normal there.
8
Q
New growth? Is it necessarily cancer?
A
Neoplasia. No, may or may not be cancer. Cancers are almost always dysplastic tissue and they are almost always neoplasias.
9
Q
Do we grow new cardiac myocytes?
A
No
10
Q
How does the heart get stronger because the cells themselves are getting bigger or because we are gaining new cells?
A
Cells themselves are getting stronger and bigger.
11
Q
What causes hypertrophy in the heart?
A
Increased PVR.
Body is stingy and is only going to adapt to what it needs to adapt too. The heart is the same way. If it has to work harder it will get stronger. If it doesn’t have to work harder it will get weaker.
12
Q
What is the difference between a power athlete that has hypertrophy in his heart and someone with AS?
A
The power athlete is only going to work a certain amount of hours per day but if someone has AS that is a 24 hour per day deal and the heart never gets the ability to rest. The heart does like to rest. It always has to beat but it doesn’t always have to beat so hard.
13
Q
What kind of cell type do bronchi and bronchioles normally look like?
A
pseudostratified columnar epithelium
14
Q
Why are the cells in the bronchi and bronchioles tall?
A
Because they have a lot of mitochondria.
15
Q
Why do the bronchi and bronchioles have a lot of mitochondria?
A
Because they have the cilia that are constantly moving gunk out of our lungs. So the ciliated columnar epithelium works great to keep our lungs nice and clean.
16
Q
After smoking normal bronchiole tissue converts to what? What kind of compensation is this? What happens if the person quits smoking?
A
Stratified squamous.
Long term compensation
The stratified squamous would convert back into the pseudostratified ciliated columnar.
17
Q
If a person continues smoking after the cells have converted to stratified squamous what could happen? Will this tissue convert back? What could happen if we pick up a couple more mutation?
A
The cells could become dysplastic. Generally, this type of tissue is not going to convert back to what it was. Unless, all the dysplastic tissue was to die and leave only the stratified squamous. Dysplasia is not cancer yet, but they have picked up a couple of mutations to be dysplastic. If they pick up a couple more mutations then it could become cancerous.
18
Q
An abnormal form of cells is known as? Give an example.
A
Dysplasia. Warts.
19
Q
A term for new abnormal disorganized growth is?
A
Neoplasia, also known as a tumor, may or may not be cancer.
20
Q
Cancers are almost always which kind of tissue?
A
Dysplastic and neoplastic.
21
Q
Name two other characteristics of cancer cells?
A
They invade and metastasize.
22
Q
For the most part, are we able to regenerate cardiac myocytes? What implication does this have on how the heart gets stronger?
A
- No.
- If the heart gets stronger it’s because the cells themselves are getting bigger and stronger not because we are gaining more cells.
23
Q
Name three reasons why a heart may become hypertrophic?
A
- increased PVR
- Aortic Stenosis
- In a power athlete
(These are just the three general ones he mentioned.)
24
Q
What is the key difference between a person with aortic stenosis and the power athlete when it comes to hypertrophy of the heart?
A
The power athlete is only going to be working a certain amount of hours per day but if someone has aortic stenosis that’s all day every day and the heart never gets the ability to rest. The heart likes to rest.
25
What is the normal cell type of the bronchi and bronchioles?
cilated pseudostratified columnar epithelium.
26
Why are the pseudostratified columnar epithelial cells of the bronchi and bronchioles so tall?
Because they have lots of mitochondria.
27
Why does the pseudostratified columnar epithelial cells of the bronchi and bronchioles have so many mitochondria?
Because of the cilia that are constantly moving gunk out of our lungs.
28
As a long term compensation for smoking the normal ciliated pseudostratified columnar epithelial cells of the bronchi and bronchioles can be converted into what cell type? What is this change called and why?
1. Stratified squamous.
2. Metaplasia because it is the change of one normal cell type to another normal cell type just not normal for the lungs.
(we normally find stratified squamous in the esophagus)
29
If a person, who's bronchi and bronchiole cells have converted to stratified squamous as long term compensation, quits smoking will this reverse?
Yes, the stratified squamous can convert back into the normal ciliated psuedostratifed columnar epithelium.
30
If a person, who's bronchi and bronchiole cells have converted to stratified squamous as long term compensation, continues to smoke what is the likely result?
At some point the cells will become dysplastic (abnormal cells that are not necessarily cancer)
31
Once a person who has smoked to the point of turning the cells of their bronchi and bronchioles into dysplastic tissue, will this reverse if the person quits smoking?
Not likely. Dysplastic tissue is generally not going to convert back to what it was. The only way this would happen would be if all the dysplastic cells were to die and leave behind only the good cells. So yeah, that's a no.
32
Dysplasia is not cancer yet, but a person who smokes with dysplastic cells has picked up a couple mutations just to become dysplastic. What does it take for these dysplastic cells to become cancer?
If the person picks up a couple more mutations then it could become cancerous.
33
When we have a cell and there is some insult a reversible cell injury can occur which could result in the cell returning to being normal or more than likely the cell will become?
Adapted- a little bit bigger or a little bit stronger
34
In an irreversible cell injury the cell just?
Dies
35
You could cut off blood supply to the heart and as long as it is returned back to the cell before the cell dies then the cell would?
Become stronger and more resistant to hypoxia.
36
If you continued to cut off blood supply to the heart but wait too long and the cell suffers and irreversible injury then?
The cell just dies and in the case of the heart it's not coming back.
37
What is the biggest cause of cell injury?
ATP depletion.
38
When we think about ATP depletion what are we really thinking of?
Ischemia
39
Why do we think of ischemia in an ATP depletion type of cell injury?
If we cut off the blood flow we are not getting any new oxygenated blood. The blood sitting around the cell isn't moving. The cell uses up the oxygen of the blood. The oxygen content of the local blood falls and then we have an oxygen deficiency which decreases the rate of ATP production in the mitochondria so now we have greatly decreased ATP.
40
If we lose the ability to use ATP what huge problem will we run into?
Lack of ATP prevents function of the Na/K ATPase pump. So we lose the ability to pump sodium out and potassium in.
41
Which causes the bigger problem, not being able to pump potassium in or not being able to pump sodium out? Why
1. Not being able to pump sodium out.
| 2. We lose our sodium gradient.
42
Why is it so important to maintain our sodium gradient?
Because with the gradient sodium wants to come back into the cell but the deal is if sodium comes back into the cell it has to bring somebody else with it or pump somebody out. So if we lose our sodium gradient we also lose our secondary active transport. Now we can't move other things around, in particular Calcium.
43
If potassium leaves the cell through leak channels and we cant pump it back in resulting in an increased extracellular potassium concentration we risk the possibility of all kinds of bad things happening because of what?
Because the of the nerst potential of potassium which in most cases largely sets the resting membrane potential for most cells. As potassium levels increase outside the cell the resting membrane potential will depolarize and to quote Garman " a permanently depolarized cell is not a happy cell"
44
What type of cell injury is particularly problematic with reperfusion? Why?
1. Free radicals and reactive oxygen species (ROS).
2. Causes oxidation of membranes and other structures.
(Oxygen likes to be reactive oxygen species, you've got to restore the blood flow when it's been cut off or the cell is going to die but when you restore the blood flow all of that incoming oxygen is going to greatly increase the oxygen reactive species in cells or in tissue that has already been partially damaged which is problematic).
45
A normal increase in intracellular Calcium is normally a signal for the cell to do what?
Whatever it does best.
46
The normal intracellular concentration of Calcium is what (generally not specific number)?
Really really really low- micromolar concentrations.
47
If a lot of calcium comes into the cell what does it signal the cell to do?
To die by apoptosis.
48
So back to the case of cell injury caused by ATP depletion. When we lose our sodium gradient we are prevented from running which pump pertinent to calcium that does what to it?
The sodium/Ca exchanger which requires ATP to pump calcium out of the cell.
49
In the case of a cardiac myocyte, if we can't pump the calcium out what happens to the contraction of the cell? What does that do to our ATP concentration? Other than losing the pump are we getting Calcium into the cell from anywhere else? What other key thing will calcium do in the cell?
1. We stay contracted longer.
2. It decreases because of the extended contraction.
3. Yes, Calcium is also being released from the mitochondria and smooth ER. (In the case of muscle cells the smooth ER is specifically adapted to be the sarcoplasmic reticulum to handle and hold calcium for contraction of the cell. We will end up releasing all of that calcium which will cause number 4.)
4. Activate a ton of enzymes.
50
How do are defects in the plasma membrane caused? What does this defect lead too.
1. Proteases and phospholipases break down the membrane.
2. If the plasma membrane starts to leak sodium is going to pour in and we are completely going to lose the sodium gradient that we've had trouble maintaining. Calcium is going to flood in as a result and cause big problems.
51
Just name the four common themes in cell injury.
1. ATP depletion
2. Free radicals and ROS
3. Increase in intracellular Ca
4. Defects in the plasma membrane.
52
In an hypoxic injury induced by ischemia we are first going to have an obstruction or cessation of blood flow that leads to ischemia. What is the first thing that is going to happen which is a huge player in the cell injury? What results from this?
1. First problem is the loss of oxygen.
| 2. The loss of oxygen is going to decrease our mitochondrial oxygenation so our ability to make ATP is going to fall.
53
When ATP falls in a normal cell what do we want the cell to do? How? How much ATP can we get during a state of ischemia?
1. Make more.
2. Increase glycolysis to get to the Kreb's Cycle to get to oxidative phosphorylation under normal conditions.
3. With glycolysis we get 2 ATPs if we don't have oxygen.
54
When we make 2 ATP after glycolysis under ischemic conditions where oxidative phosphorylation isn't possible what do we end up forming a lot of on the side? Why? What will end up binding to this side product? Resulting in what? Which could eventually lead to what?
1. We end up forming a lot of H+
2. Because under normal conditions, during oxidative phosphorylation, oxygen would react with this H+ to make H2O.
3. They will bind to pyruvate.
4. The production of lactic acid.
5. Lactic acidosis and a decrease in pH
(Just remember that the pH is not the problem. Even if we correct the pH we are still not making ATP)
55
During an ischemic conditions is any new glucose coming into the cell? So then what do we do in our attempt to compensate for low ATP?
1. No
| 2. We use all of the glucose that is there and then we are going to break down whatever glycogen is stored in that cell.
56
Do cardiac myocytes store a lot of glycogen? What about fat? Meaning what?
1. No
2. No.
3. They need a constant influx of energy but whatever little they have they are going to break down.
57
If blood flow is restored during an ischemic cell injury, the local acidosis is washed away and everyone is happy. Unless, the pH gets low enough for us to see what two things?
1. Nuclear chromatin clumping
| 2. Increased swelling of lysosomes.
58
During an hypoxic cell injury induced by ischemia, if we cannot compensate for the decrease in ATP by making more and lose the function of our sodium gradient because of sodium rushing in, what is going to follow sodium in? Causing what?
1. Water.
| 2. Acute cellular swelling.
59
Lack of ATP is also going to reduce our ability to make new proteins. Our rough ER is not going to work well. Decreased protein synthesis is going to lead to increased what? And consequently what?
1. Protein breakdown.
2. Membrane damage and if the rough ER and ribosomes aren't functioning to place the membrane damage then the cell will start to fall apart.
(The rough ER and ribosomes make protient but stop when there is no ATP)
60
When we start to lose the plasma membrane of a cell what happens to the contents? Name three of the contents we are concerned with. What happens to the calcium concentration?
1. Proteins that are in the cytoplasm are going to leak out.
2. creatine kinase, lactate dehydrogenase, troponin
3. Calcium is going to start flowing in and this is the one we really care about. If we tear up that membrane where there once was an 10000x gradient it's going to flood in.
61
What are lysosomes normally responsible for? What would happen if one swelled so much during an hypoxic injury that it burst inside the cell?
1. They digest stuff after fusing with the endocytotic vesicle.
2. It would start auto-digesting the cell.
62
What kind of cell injury includes swelling with blebs, ribosomes detaching from the ER, nucleus is clumping, some swelling of the mitochondria and lysosomes are eating cellular parts but not the entire cell?
A reversible cell injury. All of this is reversible.
63
What kind of cell injury involves lysis of the ER, the DNA inside the nucleus has been chopped up, lysosomes are rupturing and autodigesting, mitochondria become defective so they are not going to make ATP and there is membrane damage in the forms of gaps?
Irreversible. This cell is going to die.
64
Low tissue oxygen level is?
Hypoxia
65
Very low tissue oxygen level (no oxygen) is?
Anoxia.
66
Low blood oxygen tension (decreased O2 saturation) is?
Hypoxemia.
67
Is it possible to have hypoxia without hypoxemia?
Yes, in anemia. (HCT could be 12 but the sat could still be 100).
68
Does hypoxemia always result in hypoxia? What is the most likely cause?
1. Yes.
| 2. Ventilation.
69
If hypoxemia isn't a result of a ventilation issue what other type of problem could it be? (name two)
1. Cardiovascular- they cant get blood to their fingertip where the sat probe is.
2. An acute local vascular problem.
70
In greek what does ischemia mean?
Stricture.
71
What do we overuse the word ischemia to mean?
The decrease in blood flow to a tissue or organ.
72
Ischemia with necrosis is an?
Infarction. Remember if nothing dies then it is not an infarction .
73
Where can we have infarctions?
Anywhere there is blood flow and the mechanism behind it is always the same, a reduction in blood flow causing necrosis.
74
The restoration of blood supply that has been cut off is? Is this always a good thing?
1. Reperfusion
2. Well we have no choice, we have to restore the blood flow but in the case where cells have started to die reperfusion is going to add insult to injury. Oxygen can be extremely dangerous.
75
What is the difference between a thrombus and an embolism?
Embolism is ambling along. Thrombus is stationary.
76
As a general rule of thumb, if we are going to get a embolism stuck someplace where would we like it to be? Why (two reasons)?
1. The lungs
2. The lung is the most resistant organism to ischemia and they are coated with heparin which breaks down clots.
Small clots are not a problem. The lungs prevent clots from getting to your system side and lodging somewhere that they can do real damage.
77
When a thrombus cuts off blood flow what happens to the cells downstream? What happens when we restore the blood flow?
1. All the problems we discussed under ischemia.
| 2. The oxygen comes in and we get ROS.
78
What is included under reactive oxygen species? Which ones are free radicals?
1. Oxygen superanion, hydrogen peroxide and hydroxol radical.
2. Oxygen super anion and the hydroxol radical.
79
Is hydrogen peroxide reactive?
Extremely. It is deadly because it oxidizes everything. The OTC hydrogen peroxide that we use for wound healing (or to induce dog vomiting) is only 1%.
80
What else produces a lot of unwanted ROS?
The mitochondria is always producing some amount of ROS because it handles a lot of oxygen during oxidative phosphorylation.
81
What does the oxygen super anion have an extra of? Is it happy? What does this result in?
1. Electron. Oxygen is not normally negatively charged.
2. No, it is looking for something else to react with and is extremely reactive.
3. It damages every molecule that it touches until it finds something to react with.
82
How do we get rid of the oxygen super anion?
We have superoxide dismutase which converts our oxygen super anion into a hydrogen peroxide and in this case hydrogen peroxide is way less reactive than the oxygen super anion.
83
How do we get rid of hydrogen peroxide?
We have something called catalase which will convert the hydrogen peroxide into water.
84
What happens if we are missing the superoxide dismutase or catalase?
Cells would undergo tremendous amount of oxidative damage causing them to die a lot sooner.
85
What is glutathione responsible for?
Glutathione is a member of our endogenous antioxidant system and it's job is to neutralize the hydroxyl radicals either converting it to water or to a hydrogen peroxide to be converted by catalase into water.
86
Which is normally depleted in acetaminophen poisoning? Superoxide dismutase, catalase or glutathione?
Glutathione.
87
What hydroxyl radical is normally negatively charged so in the ROS what has happened?
It has lost an electron but still has an unmatched electron.
88
When do we make hydrogen peroxide in our immune cells?
When we want to kill things.
89
What are the three major antioxidant enzymes?
Super oxide dismutase, catalase and glutathione.
90
Clean controlled death is called what?
Apoptosis.
91
Messy uncontrolled cell death is called what?
Necrosis
92
If a cell is signaled to die through apoptosis what happens?
It breaks up into these little apoptotic bodies and these apoptotic bodies are like bite size morsels for some phagocyte (macrophage, neutrophil or another epithelial cell) which eat them.
93
What kind of affinity do macrophages have for apoptotic bodies?
High.
94
Under apoptosis do the cytoplasmic parts leak out of the membrane compartment? Do we see cell damage? Is this inflammatory?
1. No, we never lost membrane integrity. The phagocyte will endocytose the entire apoptotic body and the cytoplasmic parts are never released to the environment.
2. No, the sign for cell damage is cytoplasmic contents leaking into the interstitial space.
3. No, our immune system responds to cell damage
95
Under necrosis do the cytoplasmic parts leak out of the membrane compartment? Do we see cell damage? Is this inflammatory?
1. Yes, the membrane ruptures and the cytoplasmic contents leak out into the environment.
2. Yes, cytoplasmic contents leaking into the interstitial space is a shear sign of cell damage.
3. Yes, if we have cell damage our immune system is going to respond.
96
What kind of necrosis results in a tissue dying but continuing to look like the original tissue only the dead version with the cytoarcitecture still intact?
Coagulative necrosis (neutron bomb).
97
When do we see coagulative necrosis?
From infarctions (ischemia) anywhere in the body except for the brain.
98
What type of necrosis results in the tissue being liquified? Does the tissue look anything like it used to? Where do we see this?
1. Liquefactive necrosis.
2. No, it has been completely destroyed. It does not look anything like the original structure.
3. In the brain after an infarction.
99
What kind of necrosis resembles cottage cheese? Why does it resemble cottage cheese? Where do we see this?
1. Caseous necrosis
2. Bacteria produce/secrete a waxy substance which produces this cottage cheese looking necrosis.
3. Characteristic of TB.
100
When fat combines with calcium to produce calcium soaps what kind of necrosis do we see? When do we see it (name two)?
1. Fat necrosis
| 2. acute pancreatitis and in breast tissue that has been damaged
101
Why is acute pancreatitis painful? What happens to calcium?
1. Painful because enzymes start digesting everything in this region.
2. As the fat gets digested the free fatty acids bind to calcium which decreases serum calcium levels.
102
Why do we see fat necrosis with damaged breast tissue?
Because as the tissue gets damaged, if there is a lot of fat, fat will leak out and bind to calcium resulting in calcification which is completely benign.
103
What types of gangrenous necrosis do we have?
Wet or dry.
104
Where does dry gangrene necrosis occur? What is typically the causal organism? Why is the patient often unable to fight it off? Who normally gets it?
1. Places that are typically dry.
2. Clostridia family
3. Blood flow is poor to the area.
4. Diabetics- who normally already have issues with PVD (so no blood flow), and neuropathy (they can't feel it).
105
Where does we gangrene necrosis occur? What is it usually caused by? When does it become a medical emergency and why?
1. Places that stay moist (or have access to blood) internal places like the intestines but also bed sores.
2. Usually caused by clostridia
3. Gas gangrene (because of the aerobic metabolism) because it produces sepsis very quickly.
106
Where do telomeres occur? What are they? What do they code for?
1. At the end of our chromosomes.
2. DNA
3. They do not code for anything.
107
Every time a cell replicates what happens to the telomere? Why?
1. It gets shorter and shorter.
| 2. This is the part of the DNA that we do not replicate when we replicate cells.
108
Normal cell's telomeres get shorter and shorter until? What is this termed?
1. A point where it is so short that the cell cannot replicate anymore.
2. Replicative senescence- the cell still functions but cannot replicate anymore.
109
You start life will how many replications per cell? What happens when you run out?
1. About 60.
| 2. You are stuck, once we get past replication we have growth arrest and we are done replicating.
110
What is a positive to having a cell that's telomere only allows it 60 replications?
If a cell starts growing out of control it can only go so far before it stops. So this is a great check to prevent cancer.
111
What does cancer have to do to make a cell which has been growth arrested continue to replicate? What does this do?
1. Turn on an enzyme called telomerase.
2. Telomerase adds a little stuff to the end of DNA each time the cell replicates making the cells telomere longer and longer with each replication.
112
Why do we need such a thing as telomerase?
In our germ cells, if our telomeres got shorter and shorter every time we made a replication and we went out and made and egg or sperm then each one we make would have a telomere that is getting shorter and shorter. So your kid would start life with one fewer cell division and then so on and so on whith each generation until people are dead before they are born.
So we turn telomerase on our germ cells so that our germ cells have the same long telomeres to start with. Stem cells will have telomerase on partially (GI tract and skin). Normal cells will not have it on.
113
Name two causes of hypernatremia.
1. Dehydration (leading and just about the only cause)
| 2. Increased aldosterone (mild).
114
What kind of problems are we looking at with hyperkalemia and hypokalemia?
Problems with electrophysiology because potassium sets the resting membrane potential of cells.
115
Could you kill someone by having a low drip of potassium on for a long time assuming that are normal otherwise?
No, they would renally excrete it. As long as we are giving them potassium at a rate their kidneys can handle you can give them an infinite amount.
116
Why do we not normally care about chloride?
Because chloride is almost never the problem. Chloride is the good citizen that does exactly what it's supposed to do. It's job is to just be the anion. We have to have the same number of cations and anions in our blood or else we would be electrically charged. We keep all the cations we need. We keep all the anions we need. We compare them and fill the rest with chloride just to match the two.
117
High protein diet causes what change in BUN? What about a low protein diet?
1. High protein diet = increased BUN
2. Low protein diet = decreased BUN
No effect on renal function in this case, BUN comes from the amino group of AA that have been de-aminated because we have used them for their energy. The more protein we eat the more protein we make.
118
If you are heavily muscular are you going to have more or less creatinine than your evil twin who is anorexic? Is this a reflection of your kidney function?
1. Higher.
2. No, muscle contains creatine, creatine breaks down into creatinine. The more muscle you have the more creatinine you produce. No effect on kidney function.
119
In regards to anion gap, if there is another anion out there and somebody has acidosis what kind of acidosis do they have? Because of an increase in acid or a loss of base which results in what?
1. Metabolic.
| 2. Increase in acid that displaces chloride and or bicarb.
120
Why is calcium unlike our other electrolytes? What does this mean as far as lab tests?
1. It is highly bound to protein.
| 2. We have to look at free vs. bound.
121
What could alter the amount of free calcium?
Increases of decreases in plasma proteins especially albumin.
122
What can high phosphate cause?
Increase in the incidence of ectopic calcifications.
123
When do we care about uric acid? Why do we not want it too low?
1. Kidney stones and gout
| 2. It is the antioxidant of our blood.
124
ALT and AST are liver enzymes within the?
Hepatocytes.
125
If ALT and AST are in the blood what does this mean?
Hepatocytes have been damaged.
126
What is the parenchymal tissue of the liver?
The hepatocyte.
127
Alkaline phosphate and GGT mark what kind of cells? What does it mean if they are elevated? What if only alkaline phosphatase is elevated?
1. Cells of the biliary ducts.
2. Cells of the biliary ducts have been damaged.
3. Could be bone breakdown from metastatic bone cancer (alkaline phosphatase is also found in the bone).
128
Bilirubin is the result of what?
Breakdown of RBSs.
129
Unconjugated bilirubin is soluble to what?
Fat soluble.
130
In regards to bilirubin, what do we start with? What happens to it?
1. We start with unconjugated.
2. It goes to the liver and gets conjugated. Conjugated is a fancy term for sticking a water molecule onto the side of it. The conjugated bilirubin gets dumped in the duodenum and comes out in the feces. It is one of the principle factors that darkens the feces.
131
Is direct bilirubin conjugated or unconjugated?
Conjugated.
132
If you see increased bilirubin what three things typically could be the probelm?
1. Liver
2. Biliary tract
3. RBC breakdown.
133
What is the most plentiful plasma protein? What kind of citizen is it? Who makes it? Why?
1. Albumin
2. Good
3. Liver
4. The liver looks at the plasma and all the proteins in there and then makes enough albumin so that the total plasma protein level is just right.
134
When looking at albumin levels what else must we consider?
Total plasma protein.
135
If total protein is low and albumin is low who isn't doing their job? Give a second possibility.
1. The liver.
| 2. Could be a kidney problem if we are peeing out albumin faster than the liver can make it.
136
If the total protein is normal and albumin is low is the liver doing the right thing?
Yes. The liver sees that we have enough of this other protein which is way higher than it should be and only making the albumin it needs. The liver is fine, but someone out there is making too much protein.
137
What is LDH? Who has it? What does it tell you when it's found in the blood?
1. A cytoplasmic protein enzyme that converts lactate to pyruvate and pyruvate to lactate.
2. Every cell that does glycolysis so every cell in the body.
3. That cells have been damaged.
138
When there is LDH in the blood does it tell you specifically where the damage occurred? How many isoenzymes are there? Who does the cardiac myocyte share the same isoenzyme of LDH with? Meaning we need to consider what?
1. No.
2. 5
3. RBCs (so elevated result could due to poor blood draws especially if we see a high concentration of potassium). 1% RBC rupture is enough to significantly increase potassium.
4. What else would be elevated? total protein. so if you get a chem panel and the LDH, K and total protein are high you are thinking bad phlebotomy.
139
Baby RBCs are called? A special stain would show they still have what? What are they still making?
1. Reticulocytes.
2. RNA and ribosomes
3. protein/hemoglobin. `
140
Do RBCs make protein?
No.
141
When do we see an increased reticulocyte count?
Anemia because we want more RBCs.
142
What is the most common protein in the blood?
Hemoglobin
143
In general hematocrit should be how many times hemoglobin? What happens if that number is way off?
1. Three times.
| 2. It means the RBCs are either small or big.
144
Mean corpuscular volume tells us what? What units is it measured in? Smaller is an indication of what? Bigger is an indication of what?
1. The size of the RBCs
2. Femtoliter (10^-15)
3. Iron deficiency anemia.
4. Pernicious anemia.
145
Does the prothrombin rely on the extrinsic or intrinsic pathway?
Extrinsic because we need tissue factor to cause the blood to clot.
146
Does the activated partial thromboplastin time rely on the intrinsic or extrinsic pathway?
Intrinsic because all they have to do is drop glass beads in there and the blood will clot when it touches anything other than endothelial cells.
147
Bleeding time is cheap and easy why? Who would do this? Is it accurate?
1. All you need to do is cut your patient and see how long it takes them to stop bleeding.
2. Hematology
3. Really accurate measure of the way they clot.
