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Cell Biology MBS > Exam 2 Review Slides > Flashcards

Exam 2 Review Slides Flashcards

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1
Q

regeneration examples

A

liver, vascular endothelium after surgery

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2
Q

hyperplagia examples

A
  • graves (hyperthyroidism)

- restenosis (SMC)

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3
Q

metaplasia examples

A
  • CPID

- smokers

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4
Q

dysplasia examples

A
  • cervix (pap smear)

- precursor to cancer

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5
Q

neoplasia examples

  • benign
  • malignant
A
  • benign: fibroids

- malignant: cancer

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6
Q

cell cycle phases

A
  • G0
  • G1
  • R point (can be sent into G0 from here)
  • S
  • G2
  • M
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7
Q

Rb

A
  • when active, binds to E2F which stops the cell from entering S phase
  • active when unphosphorylated
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8
Q

mitogen

A

-binds to receptor and causes phophorylation of Rb by Cylcin D/e and CDK 2/4/6

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9
Q

Cyclins D and E

A

drive through the R point by phosphorylating Rb

-they work with CDK 2/4/6

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10
Q

tissues or organs the are not growing must have equal amounts of

A

-apoptosis and cell division

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11
Q

growth/shrinking rate of a tissue is determined by..

A

-the proliferation to apoptosis rate

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12
Q

necrosis

  • trigger
  • morphological changes
  • end result
A
  • ischemia, physical or chemical trauma
  • cell swells, organelles damaged, chromatin randomly degraded
  • cell lyses, organelles destroyed
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13
Q

apoptosis

  • trigger
  • morpholigical changes
  • end result
A
  • specific signals that activate genes
  • cell shrinks, organelles stay intact, chromatin degrade systematically
  • membrane blebs, cell contents retained
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14
Q

immunologically privileged sites

A
  • endothelial cells express Fas LIGAND so that they can induce apoptosis in lymphocytes so that inflammation does not occur in this region
  • eyes and testis
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15
Q

cadherin

A

-blistering disease

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16
Q

integrin disease

A

-glanzman’s thrombasthenia

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17
Q

MMP disease

A

metastatic cancers

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18
Q

collagen cross-linking disease due to copper def

A

Menke’s

-this is due to inneficient copper absorption

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19
Q

collagen 2 or chondroitin PG’s disease

A

chondrodysplasias

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20
Q

auto-immune collagen 4 disease

A

goodpastures

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21
Q

collagen 4 disease

A

alport

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22
Q

collagen 1 mutation disease

A

ehler danlos

23
Q

collagen 1 diseases

A

osteogenesis imperfecta

24
Q

collagen synthesis/cross-linking disease

A

scurvy

25
Q

fibrillin/elastin cross linking disease

A

marfans

26
Q

angiogenesis disease

A

MMP’s

27
Q

where are these collagen types found?

-1, 2, 4, 18

A
  1. ubiquitous; fibril
  2. cartilage, vitruous humor of the eye; fibril
  3. basal lamina; network
  4. basal lamina of blood vessels
28
Q

endostatin

  • used for
  • how is it made
A
  • new biology of anti-cancer chemotherapies
  • cleaved from collagen 18 by an MMP
  • is now used in 3 mil cancer patients
29
Q

leukocyte rolling and stopping

A
  1. they roll along endothelium via weak on-off interactions of carbohydrates on the leukocyte membrane with P-selectin (a matricellular protein) on the endothelium
  2. leukocytes “stick” and extravasate into inflamed areas due to PAF-activated integrins on the leukocyte binding strongly to ICAM-1 (a cell adhesion molecule) on the endothelium
30
Q

timeline of male gametogenesis

A
  • lean mean sperm making machines from puberty until death

- we have immature spermatogonia (2n) in the testes awaiting their testosterone induced awakening at puberty

31
Q

female gametogenesis

  1. 8-20 weeks of gestation
  2. birth
  3. puberty
  4. ovulation
  5. fertilization
  6. menopause
A
  1. progenitor germ cells (oogonia) become primary (immature) oocytes arrested in prophase of meiosis 1
  2. same as 20 weeks of gestation: primary oocytes arrested in prophase of meiosis 1
  3. ovaries still contain mostly primary oocytes that are now cpable of developing into secondary oocytes arrested in metaphase of meiosis 2and ready for oculation during the menstrual cycle. Only about a dozen secondary oocytes will be in the final race to be ovulated during each menstrual cycle. However, until menopause, the vast majority of oocytes will still be in prophase of meiosis 1
  4. secondary oocyte arrested in metaphase of meiosis 2
  5. membrane fusion stimulates oocyte to complete meiosis 2
  6. end of fertile period, no more oocytes are fit to be fertilizes (age 48-55)
32
Q

sperm capacitation

A
  • freshly ejaculated sperm are unable to fertilize and require this process
  • the glycoprotein coat and seminal proteins are removed from the acrosome surface
  • capacitated sperm are more active and can undergo the acrosome reaction
33
Q

acrosome reaction

A
  • the receptor for ZP3, one of -the zona pellicuda glycoproteins, is the primary sperm receptor that induces the acrosome reaction
  • this causes the release of enzymes that break down the matrix and permit sperm penetration through the follicular cells and the zona pellucida
34
Q

fusion

A
  • plasma membranes of the oocyte and sperm fuse
  • this is the eureka moment and the official start of fertilization
  • the oocyte then completes meiosis 2 and becomes a finished gamete
35
Q

cortical reaction and the block to polyspermy

A
  • sperm-oocyte membrane fusion triggers rapid and massive exocytosis of the cortical granule contents
  • the zona pellucida is then modified through proteolysis and protein cross-linking via lysosomal enzymes released from the cortical granules
  • this is mediated by Ca++
  • this produces a block to polyspermy
36
Q 
timeline of early human development 
-1
0
1
2
2.5-3
3-4
4-14
15-17
A

-1 eureka moment (fusion)
0 fertilization complete (pronuclei fuse)
1 2-cell embryo
2 4-cell embryo
2.5-3 8 cell embryo (embryo biopsy stage in PGD)
3-4 Morula (compaction; first differentiated cells)
4-14 blastocyst (implantation period)
15-17 gastrula (3 germ layers form)

37
Q

spontaneous abortion (miscarriage)

A
  • the overall earl miscarriage rate is 50%
  • most spontaneously aborted embryos that have been studied were grossly abnormal
  • major causes of early (first trimester) spontaneous abortion: chromosomal abnormalities, cleavage problems, progesterone insufficiency
38
Q

types of uterine abnormalities

A
  • uterine fibroids
  • congenital uterine developmental anomalies (Mayer-Rokitansky-Kuster-Hauser syndrome)
  • excessive scar tissue (ashermans)
39
Q

uterine fibroids

A

-benign neoplasias of uterine smooth muscle

40
Q

congenital uterine developmental anomalies (Mayer-rokitansky-kuster-hauser syndrome)

A

-could be a complete absencee of a uterus

41
Q

excessive scar tissue

A
  • ashemans

- occurs due to surgery

42
Q

causes of abnormally low sperm and low sperm number and poor sperm function

A
  • hormonal abnormalities involving the HPT axis
  • abnormally high testis temp due to varicocele in the scrotum (dialted vessels)
  • damage to , or congenital loss of, the vas defrens
43
Q

advanced maternal age for women is the leading risk factor for
-recent advances

A
  • infertility
  • spontaneous miscarriage
  • birth defects
  • however recent advances in oocyte preservation will help ameliorate the aging issues and will likely have the biggest impact on reproductive behavior since The Pill
44
Q

treating explained infertility:

  • if it is varicocele, fibroids, orashermans, or endometriosis
  • if it is PCOS
  • if the sperm are immotile,
  • -if the couple has no trouble getting pregnant but the woman has miscarriages
  • if a defect in GnRH production by the hypothal is detected
  • if the woman has gone through menopause
  • for stress or extreme athletic activity
A
  • do surgery
  • prescribe FSH
  • you need to do IVF using ICSI
  • prescribe progesterone
  • prescribe GnRH
  • then only adoption or donor egg IVF are options
  • advise a lifestyle change
45
Q

treating unexplained infertility:

  • first things first
  • if what then what…
A
  • consider the age of the woman
  • if she is over 35, go straight to IVF as the fertility will decline rapidly
  • if under 35, start her on clomiphine treatment, probably with IUI, and go on from there to add in more complex, expensive, and invasive options
  • always consider the best interest of your patient before jumping straight to these guidelines
46
Q

reprogramming cells to become iPS cells

A
  • transfect with 4-6 transcription factors

- transfecting 4-6 transcription factors will reset their genetic program to the ES cell state

47
Q

anti-angiogenesis is promoted by what?

A

collagen 18 to endostatin

48
Q

acrosome is derived from

A

-the golgi

49
Q

ashermans vs STI scarring

A
  • ashermans can be corrected with surgery

- STI’s can only be fixed if you can cure the infection which is not commmon

50
Q

kartageners and infertility

A

-kartageners aka immotile cilia disease aka primary cilia dyskinesia can cause infertility because the sperm will not be able to swim

51
Q

G1 and cyclins/CDKs

A

-Cyclin D with CDK 4/6

52
Q

G1 and S and cyclins

A

Cyclin E with CDK2

53
Q

S phase and its cyclin

A

cyclin A with CDK 2

54
Q

M phase

A

-cyclin B with CDK 1

Cell Biology MBS (22 decks)

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