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Block 4; Week 2-Michelle > Cell injury, adaptation, & death-Parks > Flashcards

Cell injury, adaptation, & death-Parks Flashcards

1
Q

What is ischemia?

A

restriction in blood supply to tissues, shortage of oxygen & glucose for cellular metabolism. Dysfunction of the tissue.

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2
Q

What is Coagulative (ischemic) necrosis?

A

Necrosis caused by hypoxia resulting from local deprivation of blood supply.

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3
Q

What is liquefactive necrosis?

A

transformation of tissue into a liquid viscous mass, associated w/ bacterial or fungal infections, cell completed digested by hydrolytic enzymes, see pus & fluid

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4
Q

What is an infarct?

A

lesion caused by tissue death b/c of lack of oxygen, b/c of restricted blood supply

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5
Q

What is (hydropic) cell swelling?

A

hypoxia can cause this (damages Na/K pump), first stage in a lot of cell injury, sometimes called hydropic change & of course the cell swells!

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6
Q

What is oxidative stress?

A

basically inability to keep up w/ reactive oxygen species. Can cause a lot of cell damage, including damage to the DNA.

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7
Q

What is lipid peroxidation?

A

oxidative degradation of lipids, messes with cell plasma membrane.

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8
Q

What is metaplasia?

A

exchange of one differentiated cell type w/ another rdifferentiated cell type.

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9
Q

What is dysplasia?

A

proliferation of immature cells & reduction in mature cells. Usu neoplastic process. Usu confined to tissue of origin.

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10
Q

What is a thrombus?

A

blood clot that hasn’t traveled anywhere, can be normal w/ injury or pathologic.

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11
Q

What is a vasospasm?

A

a blood vessel’s spasm that leads to vasoconstriction.

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12
Q

If you had a woman that presented to the clinic with acute abdominal pain & you discovered it was acute appendicitis…what would you do next?

A

Take out the appendix, of course!
Wash out the abdomen with saline.
Give her antibiotics if the appendix was perforated.

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13
Q

What might the removed appendix look like?

A

Swollen
Exudate
Perforated acute appendicitis
Fecalith obstructs the appendix, hemorrhage over the surface–>both cause inflammation

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14
Q

As a doctor, what are the 6 questions you want to ask yourself when you see a patient?

A
  1. What cells are being injured?
  2. What is the etiology of the injury?
  3. How can I stop the cell injury?
  4. How can I contain the damage?
  5. How can I clear/remove the damaged cells?
  6. How can I help the tissue repair itself & bring it back to normal function?
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15
Q

What is the difference b/w necrosis & apoptosis?

A

Necrosis: accidental cell death
Apoptosis: programmed cell death

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16
Q

Describe the cell injury path.

A

Cell has chronic stress & it adapts.
If the cell can’t adapt, it may be reversible or it may die.
Cell has injury & it is damaged.
If the injury is mild, it returns to normal function.
If the injury is irreversible, it dies thru necrosis or apoptosis.

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17
Q

What types of adaptations are possible for a cell when it experiences a chronic stress?

A 
hypertrophy
atrophy
hyperplasia
metaplasia
dysplasia
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18
Q

How did Arnold Schwarzneggar get his muscles?

A

He worked them out a lot (chronic stress) & they adapted via hypertrophy. They became swollen.

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19
Q

What is an example of chronic stress & adaptation for a human heart?

A

HTN–acts like diffuse vasoconstriction & makes it harder for the heart to pump–>this is the chronic stress.
Adaptation: hypertrophy of the heart, esp the left ventricle. The cytoplasm & nucleus enlarge.

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20
Q

What is an example of a reversible injury to the heart?

A

Ischemia, lack of blood flow. This can be recovered from, but unfortunately it makes MI more likely.

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21
Q

What is an example of an irreversible injury to the heart?

A

MI

Ischemic Coagulative Necrosis

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22
Q

What is idiopathic hypertrophy?

A

this is what happens when for whatever reason young athletes have crazy large hearts & then randomly have a heart attack in the middle of a game or something & tragically die. Idiopathic b/c people don’t know why this happens.

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23
Q

What is disuse atrophy?

A

maybe a patient just got their cast off & they see that their calf muscle is crazy small! This is b/c they didn’t use the muscle…their cells shrink. Now, they need some physical therapy to get that muscle active again.

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24
Q

What is hormonal withdrawal atrophy?

A

Decreased pituitary gland output, decreased ACTH, decreased stimulation of the adrenal gland & less androgens…cause atrophy of muscles.

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25
Q

What is cerebral atrophy?

A

this can be caused by old age or Alzheimer’s…the cells die (but still called atrophy)
decreased numbers of neurons & glial cells
gyri are smaller than normal

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26
Q

What is the difference b/w hypertrophy & hyperplasia? Which one concerns you in terms of cancer possibilities?

A

Hypertrophy: cells get larger
Hyperplasia: you get more cells
Hyperplasia is concerning in terms of cancer…

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27
Q

What is endometrial hyperplasia?

A

this is where the cells of your endometrium proliferate & you get more glands & stroma….the glands are larger, more open, & have a more convoluted border.
with this: you get abnormal bleeding–>either super heavy periods or post-menopausal bleeding. Can lead to anemia
**common in anovulatory cycles, unopposed estrogen

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28
Q

What is psoriasis?

A

this is epidermal hyperplasia-an increase in the number of squamous cells
cosmetic issues of plaques on skin
can happen b/c of chronic inflammation

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29
Q

What is metaplasia? What is an example where you have metaplasia in the lungs?

A

Metaplasia: one type of differentiated cell is replaced by another type of differentiated cell.
chronic smoker irritates the ciliated columnar epithelium. It becomes squamous epithelium. Called squamous metaplasia. What is bad about this? lose the cilia to clear out the lungs.

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30
Q

Sadly, what is the usual sequence of lung cancer?

A
  1. squamous metaplasia
  2. dysplastic squamous cells near basement membrane (messed up nuclei & stuff)
  3. full thickness dysplasia
  4. squamous cancer (non-invasive)
  5. invasive squamous cancer.
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31
Q

What is the fate of cells that have undergone metaplasia?

A

If the stressor is removed (quit smoking)…the cells may return to normal.
If the stressor isn’t removed…goes to dysplasia & maybe to cancer.

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32
Q

How does Barrett’s esophagus relate to metaplasia?

A

Reflux: gastric juice go up thru the gastroesophageal jcn & irritate the squamous epithelium (pt experiences heartburn). After a while, this undergoes glandular metaplasia & becomes glandular epithelium. Called Barrett’s esophagus.

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33
Q

What is the risk/cost of the adaptation of metaplasia in the example of reflux?

A

The glandular metaplasia could go into dysplasia & then into esophageal adenocarcinoma.

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34
Q

When you think dysplasia, think _________.

A

pre-malignant.

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35
Q

Describe 2 pathways to get from a normal cell to a cancerous cell. Note: you almost never go straight from a normal cell to a cancerous cell. Takes a pat.

A

Pathway #1: Normal cell–>Hyperplastic cell–>Cancerous Cell

Pathway #2: Normal cell–> Metaplastic cell–>Cancerous cell

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36
Q

Describe the effects of a pulmonary embolism.

A

A thrombus arose in a leg vein.
It broke off the leg vein & went into venous circulation.
It went thru the right heart & came out into the pulmonary artery where it got stuck in a branch.
It caused acute, severe ischemia of the lung.
This causes ischemic necrosis of the lung parenchyma & is called a pulmonary infarct.
Wedge-shaped hemorrhagic pulmonary infarct. (on autopsy looks darker & triangular)

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37
Q

In the case of the pulmonary wedge-shaped infarct…what does it mean that there was an infarct? What does the infarct cause?

A

Infarct: area of necrosis
Specifically: Ischemic (coagulative) Necrosis

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38
Q

What are the 2 ways that you can get ischemia?

A

Vasospasms (like how cocaine causes coronary artery vasospasms)
Thrombus

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39
Q

What is the difference b/w necrosis & apoptosis?

A

In the process of necrosis, the cell swells (its organelles & everything) until it finally starts leaking out or pops. This triggers inflammation.
As apoptosis is programmed cell death, it does NOT cause inflammation. In this case, the cell fragments are phagocytized.

40
Q

In ischemia, you have no _____ getting to the tissue. What is the problem with this?

A

oxygen!
the problem is that oxygen takes electrons & turns them into water in oxidative phosphorylation
if there is no O2, there is eventually no ATP.

41
Q

You have ischemia. You have oxygen & glucose depletion. What happens to the cell next?

A

Without O2, no oxidative phosphorylation. ATP drops.
Glycolysis kicks in to get a few ATP.
Byproduct of glycolysis is a lot of lactic acid.
pH drops.
You have a bunch of excess hydrogen ions floating in the cell…use the sodium hydrogen exchanger.
Now, you have a bunch of sodium in the cell.
You can’t use the sodium potassium pump to get rid of the extra Na+ b/c you don’t have ATP.
Use the sodium calcium exchanger instead.
Now, you have a bunch of calcium in the cell…(Ca++ also comes out of the ER & mitochondrion).
Mitochondrial calcium overload
Mitochondrial Permeability Transition
**the effects of MPT will be discussed later

42
Q

Which particles are found in the cell during ischemia? What is the problem with this?

A 
Na+
Ca++
Lactic Acid
Inorganic Phosphate
**problem: via osmosis, this will draw a lot of water in. The cell will swell and pop via necrosis.
43
Q

You take way too much Tylenol & you experience liver damage. What happens next?

A

The hepatocytes are injured & they start to swell. This is called hydropic swelling. This precedes necrosis.

44
Q

You get into a motorcycle accident & rupture your aorta. What happens to your brain?

A

Your brain doesn’t get enough blood.
Ischemia of the tissue of the brain.
Necrosis of the tissue of the brain.
Inflammation & diffuse cerebral edema.

45
Q

Describe the sequential development of biochemical & morphologic changes after cell injury.

A 
A patient may have a pulmonary infarct. They experience loss of function immediately. It takes time to experience everything else. They come in this order:
biochemical alterations (cell death)
ultrastructural changes
light microscopic changes
gross morphologic changes
**Clinical significance: X-ray may not show evidence of pulmonary infarct right away...it may take some time.
46
Q

Describe how an infarct of the small bowel could occur & what that tissue would look like on autopsy.

A

Child experiences volvulus around their SMA. this cuts off the blood supply to their lower bowel. The child experiences intense abdominal pain & shock.
On autopsy: the small bowel looks dilated, gangrenous, & hemorrhagic.

47
Q

Why does tissue that has experienced ischemia look red on autopsy?

A

b/c the tissue isn’t getting fresh blood w/ oxygen…but tissues are dying off, including the endothelial cells of the blood vessels. Old blood starts leaking out everywhere & creating that appearance.

48
Q

Coagulative/Ischemic necrosis is seen in:

A

occlusion of vascular supply

49
Q

Liquefactive necrosis is seen in:

A

in the brain, in infections

50
Q

Caseous necrosis is seen in:

A

tuberculosis

51
Q

Gummatous necrosis is seen in:

A

syphilis

52
Q

Fibrinoid necrosis is seen in:

A

HTN & vasculitis

53
Q

How does tissue that has experienced coagulative necrosis look vs. tissue that has experienced liquefactive necrosis?

A

Ischemic Necrosis:
cells swell, membranes break, cell dies. But the cells look sort of intact.
Liquefactive Necrosis:
Your tissue is liquefied & doesn’t look normal anymore. May see a fungus ball or an abscess with purulent exudate with a fibrous wall.

54
Q

What are some examples of situations where a patient would experience liquefactive necrosis?

A

AIDs patients who are immunocompromised get fungal infections, perhaps of the kidney.
Pneumonia.

55
Q

Describe what caseous necrosis looks like. What can you call this if you’re being silly? What does a patient with this type of necrosis have?

A

It looks like cheese & it is yellowish-white.
You can call it cheesy necrosis.
They have TB for sure!
**Note: microscopically you would see granulomatous inflammation.

56
Q

If you have TB where might your caseous necrosis be found?

A

It could be found in a variety of organs.

57
Q

What is something that can give you a splenic infarct?

A

infectious mono

58
Q

What are the effects of too much calcium in the cell after ischemia?

A

Ca++ activates phospholipases (this means plasma membrane, ER membrane, mitochondrial membrane will be compromised)
Proteases are activated–messes w/ the cytoskeleton
Endonucleases are activated–messes w/ DNA
ATPases are activated–reduces ATP stores
MPT (mitochondrion no longer able to make ATP)

59
Q

What is MPT? What is the problem with this?

A

Mitochondrial Permeability Transition
**the opening of pores in the mitochondrion so that stuff leaks in & out.
These are high conductance pores.
It uncouples phosphorylation & no more ATP can be made.
This means loss of membrane potential.
It also means necrosis.
Cytc will also be released from the mitochondrion, which may initiate apoptosis.

60
Q

In a healthy state do we make any free radicals? how are they formed?

A

Yes, about 5% of molecular oxygen consumed in the mitochondrion is converted into free radicals. They are formed when O2 steals electrons in the ETC.

61
Q

What are the free radicals?

A

superoxide
hydrogen peroxide
OH*

62
Q

Where does the O2 steal electrons in the electron transport chain to become ROS?

A

@ Complex I

@ Coenzyme Q

63
Q

What are some examples of anti-oxidants? Should patients always take these?

A

Vitamin E
Vitamin A
Beta Carotene
**patients shouldn’t always take them, like if they are smokers–>it could cause dysplasia.

64
Q

What are some enzymes that can neutralize free radicals & prevent cell injury?

A

SOD: super oxide dismutase (superoxide–>hydrogen peroxide)
Catalase: takes hydrogen peroxide–>H2O
Glutathione Peroxidase: takes OH*–>hydrogen peroxide
**other things: ferritin, Vit C, ceruloplasmin

65
Q

What are the free radical neutralizers that are found in the mitochondria?

A

SOD

Glutathione peroxidase

66
Q

What are the free radical neutralizers that are found in peroxisomes?

A

catalase

67
Q

What are the free radical neutralizers that are found in the cytosol?

A 
SOD
Vit C
Glutathione Peroxidase
Ferritin
Ceruloplasmin
68
Q

What is reperfusion injury?

A

When you experience ischemia & you reintroduce oxygen, you can get a lot of formation of free radicals.
ATP breaks down to hypoxanthine.
Hypoxanthine via xanthine oxidase & more O2 becomes ROS.

69
Q

Where do you get xanthine oxidase from?

A

this comes from xanthine dehydrogenase

it becomes xanthine oxidase in the presence of a lot of calcium & proteases. Note: this is the environment of ischemia.

70
Q

What is oxidative stress?

A

When the ROS are higher than the amount of anti-oxidants.

71
Q

With reintroduction of oxygen we often get more ROS…what is the problem with more ROS in the cell? How does this compound the problems we had with calcium?

A

ROS causes lipid peroxidation. This causes breakdown of membranes of the cell, nucleus, ER, mitochondrion…This also allows leakage of things into the cell (more calcium!) & out of the cell. The last thing you want is more calcium, b/c that activates phospholipases & causes breakdown of the membranes too!!

72
Q

How is lab work helpful with cell damage?

A

So…say you have ischemic tissue. If there are ROS causing membrane damage & leakage of enzymes out of the cell…w/ lab work you will be able to see the evidence of this!

73
Q

Describe the relationship b/w infarct size & reperfusion.

A

So…when a blood vessel is occluded by a thrombus…there is an area that can be salvaged (penumbra) & an area that will experience necrosis no matter what you do (distant to b.v.).
The entire area it supplies can become an infarct if not reperfused.
If reperfused, there is an area that will still infarct (bigger than necessary) and an area that will be salvaged (less than the original penumbra).

74
Q

Why does a larger area infarct than is absolutely necessary w/ reperfusion?

A

b/c of the production of ROS w/ reintroduction of oxygen. This causes lipid peroxidation & MPT. Can also contribute to calcium overload & can bring in acute inflammatory cells.

75
Q

Does the reperfusion injury area die off right away or does it take a while? Why?

A

It takes a little while. This is b/c the area that dies off via reperfusion injury usu dies via apoptosis.

76
Q

Describe apoptosis.

A

programmed cell death
orderly way to die
cell contracts instead of blowing up
little segments of the cell pop off (apoptotic bodies)
Phagocytes eat them
Note: you can sometimes see the apoptotic bodies in a flow cytometer

77
Q

T/F Less tissue dies w/ reperfusion & cardioprotection than with reperfusion alone.

A

True. This helps prevent reperfusion injury.

78
Q

How does percutaneous coronary intervention relate to reperfusion injury?

A

If you have athersclerotic coronary arteries…sometimes you use PCI to unblock these arteries. Then you get reperfusion & reperfusion injury b/c of ROS & calcium overload.

79
Q

What are the 2 forms of apoptosis? Briefly describe each.

A

Mitochondrial Pathway (intrinsic):
Bcl sensors are activated.
Bax/Bak channel is placed in mitochondrion.
Cytc & pro-apoptotic proteins are released.
Caspases are activated
Death Receptor (extrinsic):
Receptor-ligand interactions
FADD domain established w/ adaptor proteins
Caspases are activated

80
Q

What triggers the mitochondrial pathway of apoptosis?

A

Growth factor withdrawal
DNA damage
protein misfolding

81
Q

What triggers the death receptor pathway of apoptosis?

A

FAS or TNF alpha

82
Q

What do the caspases do?

A

They cause the breakdown of the nucleus & cytoskeleton.

83
Q

What is a clinical example of the extrinsic pathway of apoptosis? Explain how it works.

A

acute viral hepatitis.
hepatocyte will display the virus or HLAI on its plasma membrane.
cytotoxic T lymphocyte will bind to these things & its FAS ligand will bind to the hepatocyte’s FAS receptor.
This causes caspase activation & apoptosis
Note: w/ this type of hepatitis, cells usu don’t die via necrosis. CTL also secrete perforin & granzyme B that can help in apoptosis.

84
Q

What are 4 examples of bad intracellular accumulations?

A
  1. Abnormal metabolism–>fatty liver (lots of lipids)
  2. Defect in protein folding–>accumulation of abnormal proteins
  3. lack of enzyme–>lysosomal storage disease: accumulation of endogenous materials
  4. Ingestion of Indigestible Materials–>accumulation of exogenous materials.
85
Q

What is an example of intracellular accumulation of lipids?

A

Fatty Liver

via too much alcohol consumption

86
Q

Explain how plaque can expand in coronary arteries when macrophages get involved.

A

macrophage engulf oxidized LDL (cholesterol)

Once the macrophages get involved, they can’t get out, so the plaque just expands

87
Q

What is an additional problem with the release of lots of calcium?

A

Calcifications!!

88
Q

Why do you need to cut off dead tissue?

A

b/c dead/necrotic tissues is a place for bacterial growth. You need to cut it off.

89
Q

What happens in acute tubular necrosis?

A

the tubular cells experience necrosis
cells fall into the lumen
they form a cast
there is a back leak of edema into the interstitium

90
Q

What happens when you have hypothermia?

A

Hypothermia–>vasospasms–>often vascular occlusion–>tissue injury/necrosis

91
Q

What do you need to treat the effects of hypothermia?

A

vasodilators & thrombolytic therapy

Goal: re-perfusion.

92
Q

Why might someone need to perform a hemicraniectomy? What is this?

A

this is a removal of a portion of the skull
Cerebral Artery Occlusion–>stroke/infarct–>cell swelling/edema–>craniectomy
Note: this portion of the skull is replaced later.

93
Q

Is a hypertrophic heart more or less likely to experience ischemia?

A

It is more likely to experience ischemia b/c there is just more mass of heart to supply blood to…

94
Q

What is the color progression of a bruise? What accounts for each step?

A

Red (initially)
Black-Blue (macrophages are getting to work)
Yellow (hemosiderin, hematoidin, other pigments)

95
Q

What is hematoidin? What is hemosiderin?

A

Hematoidin: this is yellow & is a breakdown product of hemoglobin
Hemosiderin: this is related to the phagocytosis of RBCs (found in macrophages); found after hemorrhage

96
Q

What is the problem with excessive iron?

A

free radicals (lipid per oxidation & cell death)
cirrhosis
liver cancer

Block 4; Week 2-Michelle (8 decks)

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