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Mechanisms of Disease Exam #1 > Cellular Response to Stress and Toxic Insults > Flashcards

Cellular Response to Stress and Toxic Insults Flashcards

1
Q

What is the major feature of hypertrophy?

A

Increase in protein synthesis.

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2
Q

What are the major features of atrophy?

A

Increased protein breakdown (autophagy and proteosomes) and decreased protein synthesis (lowered metabolic activity).

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3
Q

What is the most common stimulus for hypertrophy of skeletal and heart muscle?

A

Increased work load.

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4
Q

Uterine enlargement during pregnancy is an example of what?

A

Hypertrophy

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5
Q

How does the heart change its energy source during pathologic conditions?

A

Before birth, carbs are the main source of energy. After birth, the “adult” isoforms of metabolic enzymes are activated and now use fatty acids.

During some pathologic conditions (hypoxia, hypertrophy, ischemia, etc), the heart returns to the “fetal” programming and use carbs again.

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6
Q

What transcription factors help induce fetal gene expression, increased synthesis of proteins, and production of GFs in a heart w/ pathology?

A

GATA4
NFAT
MEF2

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7
Q

Under what circumstances does physiologic hyperplasia occur?

A
  1. When there is a need to increase functional capacity of hormone sensitive organs.
  2. When there is a compensatory need to increase after damage or resection.
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8
Q

What are examples of physiologic hyperplasia?

A

Proliferation of breast glandular tissue (along w/ hypertrophy).
Bone marrow making more BCs.
When part of liver is resected.
When a kidney is removed, the other can be hyperplastic.

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9
Q

Viral infections, like papillomaviruses, are masses of what?

A

Masses of hyperplastic epithelium.

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10
Q

What pathway is the main degredation pathway in atrophy?

A

Ubiquitin-proteasome pathway

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11
Q

What is the mechanism of metaplasia?

A

A change in phenotype of the underlying stem cells in response to a stimulus (GFs, cytokines, environment, etc.).

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12
Q

What are the 4 examples of metaplasia given?

A
  1. Squamous metaplasia in the respiratory tract.
  2. Columnar metaplasia in the esophagus (Barret’s esophagus).
  3. CT metaplasia - formation of CT, bone, or adipose in tissues where they don’t usually exist. Usually due to intramuscular hemorrhage.
  4. Squamous metaplasia in the ducts/glands of salivation, pancreas, etc, which are usually columnar.
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13
Q

What does a vitamin A deficiency induce?

A

Squamous metaplasia in the respiratory epithelium.

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14
Q

What allows for loss of cardiac enzymes (biomarkers) during an MI?

A

A disruption of the PM in necrotic muscle cells due to the infarct. Can be detected approx. 2 hrs post cell necrosis.

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15
Q

Necrosis

Cell size:
Nucleus:
PM integrity:
Cellular components:
Adjacent inflammation?
Physiologic or pathologic?
A

Cell size: enlarged.
Nucleus: pyknosis, karyolysis, karyorrhexis.
PM integrity: disrupted.
Cellular components: enzymatic digestion. Components may leak out.
Adjacent inflammation? Yes.
Physiologic or pathologic? Pathologic.

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16
Q

Apoptosis

Cell size:
Nucleus:
PM integrity:
Cellular components:
Adjacent inflammation?
Physiologic or pathologic?
A

Cell size: smaller.
Nucleus: fragmented into nucleosome-sized fragments.
PM integrity: intact, but may have altered structure (especially in lipid orientation).
Cellular components: No leakage, but may produce an apoptosome.
Adjacent inflammation? No.
Physiologic or pathologic? Mostly physiologic, but can be pathologic.

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17
Q

Pyknosis
Karyolysis
Karyorrhexis

A

Pyknosis - nuclear shrinkage and DNA condensation.
Karyolysis - nuclear fading. DNases and RNases degrade chromatin.
Karyorrhexis - nucleus fragments.

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18
Q

Increased eosinophilia is seen in which cells?

A

Necrotic cells due to loss of cytoplasmic RNA and an increase in denatured cytoplasmic proteins, which bind eosin.

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19
Q

What are key features of Coagulative Necrosis?

A
  • Due to ischemia from infarct.
  • Architecture of cells is preserved for a few days, but then removed by phagocytosis by WBCs.
  • Firm texture.
  • Often wedge-shaped.
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20
Q

What are key features of Liquefactive Necrosis?

A
  • Usually due to hypoxic death of cells in the CNS and the digestion of them.
  • Can be seen in bacterial and sometimes fungal infections.
  • Looks creamy yellow, like pus.
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21
Q

What are key features of Gangrenous Necrosis?

A
  • Necrosis of the limb (usually coagulative) involving multiple tissue planes.
  • Not a specific death pattern.
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22
Q

What is wet gangrene?

A

Bacterial gangrenous necrosis superimposed (more liquefactive necrosis) on gangrenous necrosis.

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23
Q

What are key features of Caseous Necrosis?

A
  • Most likely in foci of TB infection.
  • Cheese-like, white appearance.
  • Structureless, but has a definitive border -> granuloma.
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24
Q

What are key features of Fat Necrosis?

A
  • Focial areas of fat destruction, due to release of activated pancreatic lipases.
  • Often in acute pancreatitis.
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25
Q

What are key features of Fibrinoid Necrosis?

A
  • Involved in immune reactions involving BVs.

- Bright pink appearnce in H/E stains.

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26
Q

What is granulomatous inflammation?

A

Chronic inflammation characterized by a collection of Mo, T cells and sometimes central caseating necrosis.

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27
Q

What are 3 major effects of ischemia on the mitochondrion?

A

MAINLY: lowers ATP, which leads to the following:

  1. Decreased activity of Na+ pump (increased influx of Ca++, water and Na+ w/ increased efflux of K+) which leads to ER swelling, cell swelling loss of micorvilli and blebs.
  2. Increased anaerobic metabolism leading to low pH and clumping of nuclear chromatin.
  3. Detachment of ribosomes which decreases protein synthesis.
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28
Q

What enzyme converts superoxide to hydrogen peroxide?

A

SOD

29
Q

What enzymes decompose hydrogen peroxide?

A

Glutathione peroxidase and catalase.

30
Q

How can superoxide dismutase become a hydroxyl radical?

A

It transitions to H2O2, then to hydroxyl radical.

31
Q

What are major implications of increased cytosolic Ca++?

A
  1. Activation of phospholipase and proteases that damages membranes and cytoskeletal proteins.
  2. Activation of endonuclease which degrades nucleus.
  3. Increases mitochondrial permeability (mitochondrial transition pore).
32
Q

What is cfDNA?

A

Cell free DNA released by tumor cells, hematopoietic and stromal cells, meaning in patients w/ cancers, cfDNA from both types circulate.
It is released by apoptotic and necrotic cells.

33
Q

What is the overview of the mitochondrial (intrinsic) pathway?

A
  1. DNA is damaged somehow (toxins, radiation, etc).
  2. Sensor proteins activated and antagonizes BCL2.
  3. Cytochrome C leaks out of mitochondrial membrane through BAX/BAK channel.
  4. Caspases are activated.
34
Q

Which proteins are anti-apoptotic? What kinds of domains?

A

BCL2, BCL-XL, MCL.

4, BH (BH1-4)

35
Q

Which proteins are pro-apoptotic? What kinds of domains?

A

BAX, BAK.

4, BH (BH1-4)

36
Q

Which proteins are sensors? What kinds of domains?

A

BAD, BIM, BID, Puma, Noxa.

1, BH3.

37
Q

What does the apoptosome do and how is it formed?

A

It activates caspace-9 (the critical initiator of mito pathway).
Formed by cytochrome C and APAF-1 binding.

38
Q

What do IAPs do?

What inhibits them?

A

They block the initation of caspases and try to keep cells alive.

Smac and Diablo inhibit them.

39
Q

Which cells are receptors on cell PMs undergoing then extrinsic pathway?

A

Fas

TNF receptor

40
Q

What is the overview of the extrinsic pathway?

A
  1. FasL (on T cells) or TNF bind their receptor.
  2. FADD is activated and activated caspace-8.
  3. Caspase-8 activated executioner caspases.
41
Q

What is FLIP?

What expresses it frequently?

A

A protein that binds to pro-caspase-8 and inhibits its activation. Therefore it inhibits the extrinsic pathway.

Virsuses express it to inhibit Fas-mediated apoptosis.

42
Q

DNA damage causes p53 to accumulate. What 4 things can it trigger?

A
  1. Senescense (can no longer divide).
  2. Activate p21,a CDK inhibitor, that causes G! arrest and allows for cell repair.
  3. Activate GADD45, which triggers DNA repair.
  4. Activate BAX and apoptosis.
43
Q

What occurs with the unfolded protein response in healthy and stressed cells?

A
  1. Slow protein synthesis and produce chaperones to correct misfoldings.
  2. Apoptosis is triggered.
44
Q

Which ones are executioner caspases?

Which ones are initiator caspases?

A

Caspase-3 and -6.

Caspase-8 and -10.

45
Q

What are some disorders associated w/ increased apoptosis and excessive cell death?

A

Autoimmune diseases
Neurodegenerative diseases
Ischemic injury (MI, stroke, etc.)

46
Q

Phases of autophagy

A
  1. Initiation
  2. Elongation
  3. Maturation of autophagosome
    4, Fusion w/ lysosome
  4. Degredation
47
Q

What is the function of LC3?

A

It is required for the elongation and closure of the autophagosome membrane.

48
Q

Dysregulation of autophagy occurs in which diseases?

A

Cancers
Inflammatory bowel diseases
Neurodegenerative disorders
Some infections (host defense mechanisms)

49
Q

Exogenous pigment accumulations

A

Anthracosis

Tattoo

50
Q

Endogenous pigment accumulations

A

Lipofuscin
Melanin
Hemosiderin

51
Q

What is hyaline change?

A

A change within cells or extracellularly that gives a glassy, pink appearnce in histologic sections in H/E stains.

It does not represent a specific pattern of accumulation.

52
Q

What is a disease associated with glycogen build up in cells?

What organs does glycogen build up in?

A

DM.

Renal tubular cells, hepatocytes, beta cells of pancreas and heart muscle cells.

53
Q

What types of patients might have buildup of anthracosis?

A

Coal worker, smoker.

54
Q

What types of patients/where might have build up on lipofuscin?

A

Aging patients in their liver and heart.
Severely malnourished.
Cancer cachexia.

55
Q

What disease may have a build up melanin?

A

Alkaptonuria

56
Q

What patient may have a buildup of hemosiderin?

A

Bruises
Iron metabolism disorders
Local hemorrhages
Anemias

Can be seen regularly in spleen, bone marrow and liver.

57
Q

Where is dystrophic calcification seen?

A

Necrotic, damage or aging tissues.

Often in heart valves.

58
Q

Where is metastatic calcification seen?

What disorders are associated with it?

A

In areas of hypercalcemia.

HyperPTH
Resorption of bone due to tumors.
Vit D disorders.
Renal failure

59
Q

What kinds of signaling counteracts aging?

How?

A

Decreased insulin/IGF signaling.
Decreased TOR.

It changes transcription to encourage DNA repair and help protein homeostasis

60
Q

What 3 things can lead to cell aging?

A 
ROS (carcinogens, sporadic errors, etc)
Telomere shortening (senescence)
Decreased proteins, damaged proteins (defective protein homeostasis.
61
Q

How does caloric restriction increase longevity? How are sirtuins involved?

A 
It lowers signaling intensity of IGF-1 pathway by increasing sirtuins.
The sirtuins (surtuin-6) contribute to metabolic adaptations of caloric restrictions and promote genomic integrity by activating DNA repair enzymes via deacylation.
62
Q

Which molecules are most important in physiological hypertrophy of the heart?

A

PI3K/AKT

63
Q

What are myelin figures?

A

They are remnants of phospholipid membranes that represent irreversible cell damage.

64
Q

What is the Fenton reaction?

A

The oxidation of Fe2+ to Fe3+ with water. It produces an OH-*.

65
Q

What is the major action of O2-?

A

To activate degredative enzymes rather than directly effect a cell.

66
Q

What is pyroptosis?

A

A good way to kill microbes in the cytoplasm.

IL-1 is released (causes fever) and activates the inflammasome which activates caspase-1 and -11.

67
Q

What are Russell bodies?

A

They are produced by distended ERs in cells that make a lot of proteins (like plasma cells and Igs).

68
Q

What has rapamycin been shown to do in rats?

A

Inhibit the mTOR pathway and increase lifespan.

69
Q

What is a psammoma body?

A

Lamellar concentrations of Ca++ seen in dystrophic calcification.

Mechanisms of Disease Exam #1 (5 decks)

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