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Cell Biology > Exam II > Flashcards

Exam II Flashcards

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1
Q

Regeneration

A

1:1 replacement of cells, with exact same cell type. Always helpful, never pathological.

Example: liver transplant. regeneration following vascular surgery

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2
Q

Hyperplasia

A

increase in # of cells in a tissue, but cells are still funcitonal. can be pathological or can be fine.

Example: hematopoietic cells in bone marrow following blood loss. Graves disease (harmful), smooth muscle cells in arterial wall of atherosclerosis.

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3
Q

Metaplasia

A

adaptive substitution of one cell type to another. Always pathological (net harm). chronic pelvic inflammatory disease, smokers

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4
Q

Dysplasia

A

pre-curser to cancer. Cells are irregular, different sizes, large nuclei. Have to remove the stimulus, or it will lead to cancer.

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5
Q

Neoplasia

A

irreversible proliferation of cells continues even in the absence of external stimulus.

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6
Q

Benign vs. malignant

A

benign: loss of proliferation controls only
malignant: loss of both proliferation and positional controls

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7
Q

What is an example of a benign neoplasia?

A

Uterine Fibroids

  • problematic in 20% of women
  • higher incidence in black women
  • only treatment is hysterectomy.
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8
Q

What causes necrosis?

A

sustained ischemia, physical or chemical trauma.

cells swell, organelles damages, chromatin randomly degraded

cells lyse, organelles destroyed

leads to inflammation

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9
Q

What causes apoptosis?

A

triggered by specific signals that activate specific genes

cells shrink, organelles intact, chromatin degraded systematically

membrane blebs, cell contents retained

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10
Q

What is syndactyly and polydactyly an example of?

A

apoptosis gone wrong

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11
Q

What is the replacement of ciliated columnar epithelium by stratified squamus epithelium in response to chronic inflammation an example of?

A

metaplasia

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12
Q

What is an abnormal pap smear an example of?

A

dysplasia

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13
Q

What happens in G1?

A

Prepares cell for replicating DNA, cell is busy doubling its contents in anticipation of division

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14
Q

What happens in S phase?

A

DNA replication

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15
Q

What happens in G2?

A

prepares cell for segregation/division of genome and cytoplasm

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16
Q

What happens in M?

A

mitosis and cytokenesis

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17
Q

What phase are 99% of cells in?

A

G0

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18
Q

Which cyclin couple regulates the M phase and what happens?

A

Cyclin B/cdk1 complex;

  1. phosphorylation of lamins
  2. phosphorylation of histones
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19
Q

What complexes have to build up to phosphorylate the Rb protein?

A

CDK4-6/Cyclin D and cyclin E/CDK2

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20
Q

What are the key features of apoptosis?

A
  1. Triggered by specific signals that activate specific genes
  2. cells shrink, organelles intact, chromatin degraded systematically
  3. membrane blebs, cell contents retained
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21
Q

What are the key features of necrosis/cell lysis?

A
  1. Triggered by ischemia or trauma
  2. cells swell, organelles damaged, chromatin degraded randomly
  3. cells lyse, organelles destroyed.

Disordered; leads to inflammation

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22
Q

Does the Bcl family of proteins modify the intrinsic or extrinsic cell death pathway?

A

Intrinsic only

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23
Q

What simulates the intrinsic growth pathway?

A

growth factor/survival factor withdrawal, glucocorticoids, viruses, DNA damage causing events, toxins, free radicals

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24
Q

What stimulates the extrinsic cell death pathway?

A

TNF or Fas ligand binding to cell surface receptors

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25
Q

What are the three key steps in apoptosis?

A
  1. inducers
  2. modulators (Bcl-2_
  3. effectors (caspases and endonucleases)
26
Q

Where do endonucleases cleave DNA in apoptosis?

A

in the linker regions between nucleosomes, or can cleave cytoskeleton proteins resulting in blebbing

27
Q

What is cachexia (wasting) in cancer patients a sign of?

A

Apoptosis (too much)

28
Q

Which tissues see the greatest frequencies of apoptosis?

A

Those with the most cell proliferation: thymus, spleen, small intestine, epidermis, ovarian follicles

29
Q

Where is type 4 collagen found?

A

basal lamina

30
Q

Where is type 2 collagen found?

A

in cartilege

31
Q

What does endostatin do and where is it cleaved from?

A

It is a powerful anti angiogeneisis protein cleaved from collagen type XVIII ( a blood vessel specific collagen)

32
Q

What is endostatin used to treat?

A

cancer and macular degeneration

33
Q

What role do proteoglycans and hyaluronan play?

A

They provide hydration and structural support for cells and act as shock absorbers. They are a reservoir for growth factors and cytokines

34
Q

Which element of the cell matrix does marfans target?

A

fibrillin (elastic fibers)

35
Q

Pemphigus (blistering disease)

A

autoAbs to cadherins

36
Q

Glanzmann’s thrombasthenia

A

integrin defect

37
Q

metastatic cancer

A

MMPs (Matric Metalloproteinases)

38
Q

Menkes disease

A

collagen I cross linking

39
Q

Goodpasture syndrome

A

autoAbs to collagen IV; affects both kidney and lungs

40
Q

Alport syndrome

A

mutations in collagen IV gene, only affects kidney

41
Q

Ehler Danlos syndrome

A

defects in collagen synthesis and fibril assembly

42
Q

Osteogenesis imperfecta

A

Mutaiton in collagen I gene

43
Q

Scurvy

A

collagen cross linking defect due to lack of vitamin C

44
Q

Angiogenesis

A

the formation of new blood vessels (Matrix metalloproteases)

45
Q

What cyclins are associated with S phase?

A

cdk2 and cyclin A

46
Q

What complexes phosphorylate the Rb protein

A

Cdk2/cyclin E and cdk4/6 and cyclin D

47
Q

Spermiogenesis key points

A
  1. acrosome is a specialized form of golgi
  2. mid piece has mitochondria to provide energy to tail
  3. sperm are produced from puberty onward
48
Q

What does FSH do?

A

stimulates ovarian follicle growth, differentiation, and steroidogenesis (mainly estrogen)

49
Q

What does LH do?

A

stimulates ovulation, corpus luteum formation, and steroidogenesis

50
Q

What does PGE2 do?

A

contracts thecal cells, expelling oocyte, blocks activation of T-ce;;s and NK cells, contracts uterus

51
Q

What does Collagen type IV do?

A

forms sheetlike networks, basal lamina

52
Q

Which proteins are involved in the rolling of the leukocyte and which are involved in sticking?

A
  1. matricellular protein (p-selectin which is on the endothelial cell)
  2. sticking and extravasation is due to integrin on leukocyte (ICAM is expressed on inflamed tissue)
53
Q

What phase are primary oocytes arrested in?

A

Prophase of meiosis 1

54
Q

What phase are secondary oocytes arrested in?

A

metaphase of meiosis II

55
Q

Chondrodysplasias

A

collagen II or chondroitin PGs

56
Q

What are matricellular proteins?

A

fibronectin, laminin, selectins

57
Q

What is the receptor on the sperm that induces the acrosome reaction?

A

ZP3 (within the zona pellucida glycoproteins) this is what is species specific

58
Q

What reaction blocks polyspermy?

A

the cortical rxn: lysosomal derivatives that cross link proteins in the zona pellucida

59
Q

Timeline of development.

What happens at day:
0?
1?
2?
3-4?
4-14?
15-17?
A

0- complete fertilization when the pronuclei fuse

1- 2-cell embryo

2- 4-cell embryo

3-4 days: Morula

4-14: Blastocyst

15-17: gastrula (3 germ layers)

60
Q

What is the difference between ashermans and STI scarring?

A

Ashermans is the uterine lining, result of surgery. STI scarring is the vaginal canal of cervix

61
Q

What is the disease w/ no uterus?

A

Mayer-rokitansky-kuster-hauser

Cell Biology (2 decks)

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