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Basic Principles Of Medicine 1-FTM 1 > Apoptosis And Necrosis > Flashcards

Apoptosis And Necrosis Flashcards

1
Q

Give 4 cell accumulation disorders

A
  • cancer
  • lupus erythematous
  • glomerulonephritis
  • viral infections
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2
Q

Give 4 cell loss disorders

A
  • AIDS
  • Alzeihmers disease
  • Parkinson’s disease
  • aplastic anemia
  • myocardial infarction
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3
Q

What are neoplasms?

A
  • “new growth”

- Abnormal mass of cells

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4
Q

What are the two main groups of neoplasms ?

A
  1. Benign neoplasms
    • Grow slowly & remain localized to site of origin
  2. Malignant neoplasms= cancer
    - Grow rapidly and May spread
    - Abnormal growth of tissue
    • Clusters of cells that are capable of growing and dividing uncontrollably
    • Growth is not regulated
    • Rapid cell proliferation ignoring normal restraints on cell division
      • Restriction of space
      • Nutrients
      • Cell cycle regulation
      • Cell death (apoptosis )
      • RES/
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5
Q

What are the hallmarks of cancer?

A
  • Tumor promoting inflammation
  • Limitless ability to reproduce
  • Ignores anti-growth signals
  • Self- sufficient growth signals
  • Avoids apoptosis
  • Sustained angiogenesis
  • Tissue invasion and metastasis
  • Genomic instability and mutations
  • Avoiding immune destruction
  • Deregulating energy metabolism
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6
Q

Briefly describe cancer nomenclature

A

Malignant neoplasms are classified according to tissue and cell type from which they originated

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7
Q

What is a carcinoma?

A
  • Malignant tumor growing from epithelial tissue

- Many carcinomas affect glands that are involved with secretion

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8
Q

What is sarcoma?

A

Malignant tumor growing from connective tissues

  • Cartilage, fat, muscle, tendons, and bones
  • Ex. Osteosarcoma (bone) and chondrosarcoma (cartilage)
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9
Q

What is leukemia?

A

Cancer of blood or bone marrow

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10
Q

What is melanoma ?

A

Malignant tumor of melanocytes

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11
Q

What is a malignant neoplasm?

A

Locally invasive

-Tumor invades the tissues surrounding it by sending out “fingers” of cancerous cells into the normal tissue

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12
Q

Explain what’s metastasis

A

Distant spread of the tumor cells into other tissues in the body

Modes:
1. Vascular - veins

  1. Lymphatic -lymphatic vessels
  2. Transcoelemic- across coelemic spaces
    - Ex. Peritoneal & pleural cavities
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13
Q

How are cancers classified?

A

Classified according to tissue and cell tyroe from which they arise

About 90% of human cancers are carcinomas
-Most of the cell proliferation in the body occurs in epithelial tissue

-Epithelial tissue frequently exposed to physical and chemical damage

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14
Q

Describe cancer growth

A
  • Origins can usually be traced to a single primary tumor
  • Derived by cell division of a single cell
  • Typical tumor can contain more than a billion cells before first detection
  • Doubling time of a typical breast tumor is about 100 days
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15
Q

Summarize tumor formation and proliferation

A

Tumor formation

  1. Clonal evolution- develops through repeated rounds kf mutation and proliferation
    - cells aquire a selective growth advantage over neighbor cells
  2. Stem cell
    - Tumors contain cancer stem cells
    - indefinite proliferative potential
    - linked initially to leukemia’s

Tumor progression

  • most human cancer cells are genetically unstable
    • defective repair of DNA damage or replication errors
    • Loss of chromosome integrity
      • abnormal karyotype
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16
Q

Contrast cell swelling and cell shrinking for necrosis and apoptosis

A

Necrosis-causes cell swelling

Apoptosis- causes cell shrinkage

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17
Q

Contrast plasma membrane related events in necrosis and apoptosis

A

Damage to plasma membrane- necrosis

Plasma membrane blabbing- apoptosis

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18
Q

Contrast Nucleus activities in apoptosis and necrosis

A

Aggregation of chromatin- apoptosis

Fragmentation of nucleus- apoptosis

Necrosis doesn’t do either

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19
Q

Contrast DNA activities in relation to necrosis and apoptosis

A

Oligosaccharide DNA fragmentation- apoptosis

Random DNA degradation- necrosis

Caspase cascade activation- apoptosis

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20
Q

How are chromosomes sorted in karyotypes?

A

Chromosomes sorted by size, shape & fluorescent Chrimoeome 1 is the biggest and first, decreased in s8ze as numbers increase

Comeback to see translocation between chromosomes 8 and 14 that. Leads to tumors

21
Q

A karyotype is made of a Breast cancer patient, what is to be expected?

A

A. General stain
-48 chromosomes rather than the normal 46

B. Fluorescent stains
-Evidence of multiple translocations

22
Q

What are the 2 general mechanisms of cell death?

A
  1. Necrosis
    - Principle outcome in many injuries
    - Ex. Ischemia, toxins, infections & trauma
  2. Apoptosis
    - Regulated cell suicide program
    - Occurs during development &throughout adulthood
    - Physiological-development, tissue homeostasis
    - Some pathological conditions (DNA Damage, Misfolded proteins, some viral infections)

Distinct morphological differences
Distinct biochemical differences

23
Q

Summarize necrosis

A
  • Pathologicial
  • Acute cell injury
  • Cell unable to maintain homeostasis
  • Cell swelling
  • Loss of plasma membrane integrity
  • Cell contents released
  • Surrounding tissue damage
  • Inflammation
24
Q

Summarize apoptosis

A
  • Physiological
  • Genetic
  • Programmed cell death
  • Cell shrinking
  • DNA aggregation
  • Maintains plasma membrane integrity
  • No surrounding tissue damage
  • No inflammation
25
Q

Describe the morphological assessment of necrosis

A

Morphological

  • Propidium iodide(PI) staining
    • Live cell imaging
    • PI intercalates & labels DNA
    • PI positive = leaky /discontinuous plasma membrane = necrosis

H&E staining

  • Increased eosinphilia
    • Loss of cytoplasmic RNA
    • Increase in denatured proteins
  • Variable nuclear staining
    - Typical loss of basophilia & total loss of nuclear staining after a couple of days; sometimes pyknosis visible

TEM
-discontinuous plasma & organelle membranes

26
Q

What are the biochemical assessments of necrosis?

A
  • Random DNA degradation

- Increased levels of lactate dehydrogenase (LDH)

27
Q

What can be contrasted from an H & E stain of the kidney in necrosis and being normal

A

Infarct- increased eosinophilia, loss of nuclei, increased inflammatory infiltrate

28
Q

What are the mechanisms of apoptosis?

A

2 pathways:

  • intrinsic
  • extrinsic

Differ in induction & regulation

Both result in activation of initiator & executioner caspases

29
Q

What is a use for apoptosis in normal e,bryological development?

A

Ex. Developing digits

30
Q

What is a use for apoptosis in normal tissue homeostasis?

A
  • Billions of cells undergo apoptosis daily

- Replaced by renewing cell populations

31
Q

What is a use for apoptosis in abnormal tissue homeostasis?

A
  • Loss of cells due to apoptosis
    • Immune deficiency syndromes, some types of anemia
  • Irreplaceable due to non-renewing cell populations
    • Ahlzeimer’s, Parkinson’s, myocardial infarction
  • Accumulation of cells due to failure of apoptosis
    • Malignant neoplasia, autoimmune syndromes
32
Q

How does apoptosis helps with indigitation?

A
  • Digits, in this case in a mouse paw are sculpted by apoptosis
  • Webbing of human toes may occur because of interrupted apoptosis
33
Q

What are the characteristics of the intrinsic pathways?

A

Death signal
-Ex. DNA damage

  • Pro-apoptotic proteins unregulated
    • Ex. Bax

-Release of cytochrome c from mitochondria

  • Apoptosome formation
    • Apaf-1
      • Apoptotic protease activating factor 1
    • Cytochrome c
    • Procaspase 9

Caspase cascade

  • Activation of initiator caspase 9
  • Activation of effector caspases
    - Ex. Caspase 3
34
Q

Summarize the steps of the intrinsic pathway

A
  1. Apoptotic stimulus triggers the mitochondria to release cytochrome c
  2. Release of cytochrome c triggers the activation of Apaf-1
  3. Apaf-1 molecules assemble together to form the apoptosome
  4. The recruitment and activation of procaspase-9 leads to binding if the CARD domain to the apoptosome
  5. This leads to activation of executioner pro caspases. Caspase cascade leading to apoptosis
35
Q

What are the characteristics of the extrinsic pathway for apoptosis ?

A

Extrinsic

  • Binding of ligand to death receptor
    • Fas ligand
  • Recruitment of death domain adaptor proteins
    • FADD
    • TRADD

-Formation of death inducing signaling complex (DISC)

  • Caspase cascade
    • Activation of initiator caspases
      • Ex. Caspase 8
    • Activation of effector or “executioner” caspases
      • Ex. Caspase 3
36
Q

Describe the extrinsic pathway

A

A killer lymphocyte presents a Fas ligand to the Fas death receptor on a cell-the inner part of the Fas death receptor holds a death domain within the cell

  1. The FADD adaptor protein contains a death domain as well and a death effector domain
  2. Procaspase 8 or 10 contains a death effector domain
  3. When the killer lymphocyte binds the target cell, this results in the assembly of DISC, the death domain of FADD receptor and FADD adaptor protein bind, also death effector domain of of lrivaspase 8 or 10
  4. The DISC includes the FADD death domain, FADD death effector domain, death effector domain in the pro caspase 8 or 19 and procsspase 8 or 10 itself
  5. Activation and cleavage of pro caspase 8 or 10 or both
  6. This leads to activation of executioner caspases and apoptosis occurs
37
Q

What are the initiator caspases?

A

Caspases 2,8,9,10- initiator caspases

38
Q

What are the effector caspases?

A

3,6,7

39
Q

What caspases are related to inflammation?

A

Caspases 4,5

40
Q

What caspases are involved in skin development ?

A

Caspase 14

41
Q

What caspase isn’t Apoptotic?

A

Caspase 1- cytosine maturation

All the others are Apoptotic

42
Q

What are caspases?

A

Family of protease enzymes
-Cysteine-dependent Aspartate-directed proteases

  • Synthesized as inactive precursors-pro caspases
  • Activated by proteolytic cleavage
  • Target cytoplasmic & nuclear proteins and caspase-active DNAse
43
Q

Describe the Bcl-2 family

A

-Intracellular regulators of apoptosis

2 functional classes

  1. Pro-Apoptotic
    • Bid- links extrinsic & intrinsic pathways
    • Bax & Bak- permeabilization of mitochondrial outer membrane
  2. Anti-Apoptotic - Bcl-2

Balance of pro- & Apoptotic proteins largely determines cell fare

44
Q

What Bcl-2 proteins are pro and anti survival?

A

Pro-survival: Bcl- 2, Bcl-xL

Anti-survival/pro-death:

  • Bax
  • Bak
  • Bid
45
Q

What role does Bcl-2 do in apoptosis ?

A
  1. Death receptor signaling results in caspase 8 activation
  2. Caspase 8 cleaves to Bid and tBid
  3. Bak and Bax can now enter the Mitichondrial membrane
  4. Cytochrome c is released from mitichondria
  5. Caspases are activated and induce proteolysis resulting in apoptosis
46
Q

Describe the assessment of apoptosis

A
  • Caspase activity
  • Annexin 5- protein binds to phosphatidylserine when exposed on the outer leaflet of the plasma membrane
  • DNA laddering
    • DNAse cleaves internucleosomal DNA
    • 180-200 bp fragments

TUNEL

  • terminal uridine deoxynucleotdyl transferase nick end labeling
  • Detects DNA fragmentation
47
Q

What is TUNEL?

A

Assay detects dna fragmentation

Tagged or labeled deoxynucleotides to 3’ DNA ends

48
Q

Who won the Nobel prize in physiology of medicine in 2002?

A

Awarded jointly to Syndeny Brenner, H. Robert Horvitz and John E. Sulston “for their discoveries concerning genetic regulation of organ development and programmed cell death”

Basic Principles Of Medicine 1-FTM 1 (39 decks)

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