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Cell Biology > Exam 2 Review Slides- Lecture 9/24/21 > Flashcards

Exam 2 Review Slides- Lecture 9/24/21 Flashcards

1
Q

Reversible proliferative states (4)

A
  • Regeneration
  • Hyperplasia
  • Metaplasia
  • Dysplasia
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2
Q

Irreversible proliferation states

A

Neoplasia=tumor

  • Benign
  • Malignant
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3
Q

Examples of regeneration

A

Liver, vascular endothelium after surgery

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4
Q

Hyperplasia examples (pathologic)

A

Graves (hyperthyroidism), restenosis (after balloon angioplasty),

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5
Q

Example of hyperplasia (physiologic)

A

Expansion of hematopoietic

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6
Q

Metaplasia examples

A

Chronic PID, respiratory epithelium in smokers

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7
Q

Dysplasia examples

A

Cervix (pap smear), precursor to cancer

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8
Q

Benign neoplasia example

A

Fibroids

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9
Q

Malignant neoplasia example

A

Cancer

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10
Q

Tissue growth

A

More proliferation than apoptosis

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11
Q

Tissue shrinkage

A

More apoptosis than proliferation

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12
Q

Necrosis hallmark

A

Inflammation, triggered by sustained ischemia, physical or chemical trauma, cells swell and lyse

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13
Q

Apoptosis hallmark

A

Phagocytosis, triggered by specific signals, cells shrink, organelles intact, chromatin degraded systematically, membrane blebs

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14
Q

3 phases of apoptosis

A

1) Induction
2) Modulation
3) Execution

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15
Q

Induction

A

Physiologic, damage-related, therapy-associated. Intrinsic and extrinsic pathway

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16
Q

Examples of extrinsic apoptosis

A

FasL (immunological privilege)

TNFalpha (tumor necrosis factor)

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17
Q

Modulation

A

Intrinsic only, pro and anti apoptotic BCL family proteins

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18
Q

Execution

A

Caspase cascade-> induces blebbing and endonuclease activity

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19
Q

Immunologic privileged sites

A

Eye and testis, endothelial cells express FAS ligand and Lymphocytes express fas receptor, induces apoptosis

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20
Q

Cacchexia

A

Mass cell death by TNF in cancer

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21
Q

Blistering diseases dysfunction

A

Keratin (desmosomes, hemidesmosomes)

22
Q

Glanzmann’s thrombasthenia

A

Integrins, platelets can’t aggregate

23
Q

Metastatic cancer dysfunction

A

Overproduction of MMPs allow metastasis, inhibiting MMPs cuts off angiogenesis

24
Q

Chondrodysplasias

A

Mutations in Collagen II or chondroitin PG

25
Q

Goodpasture syndrome

A

Autoimmune disease attacks collagen IV, affects lung and kidney basement membrane

26
Q

Alport syndrome

A

Collagen IV mutation, effects the kidney

27
Q

Ehler-Danlos syndrome

A

Various collagen mutations, hyper flexible joints, loose skin, etc

28
Q

Osteogenesis imperfecta

A

Collagen I mutation

29
Q

Scurvy

A

Vitamin C deficiency, cofactor needed for prolylhydroxylase in collagen synthesis

30
Q

Angiogenesis

A

MMP involves, especially collagen XVIII

31
Q

Anti-angiogenesis

A

Endostatin derived from collagen XVIII inhibits MMPS, stops angiogenesis

32
Q

Collagen I

A

Most abundent, fibrillar, found in bone tendon, CT etc

33
Q

Collagen II

A

Fibrillar, found in cartilage

34
Q

Collagen IV

A

Sheet like network, found in the basal lamina

35
Q

Collagen XVIII

A

Found in the basal lamina around blood vessels

36
Q

P-selectin

A

A matricellular protein that aids in leukocyte “rolling”

37
Q

ICAM-1

A

Cell adhesion molecule 1, beinding to this molecule triggers extravasation

38
Q

Male timeline of spermatogenesis

A

From 20 weeks of gestation until puberty, have immature spermatogonia, after puberty make a ton of sperm

39
Q

Female timeline of gametogenesis

A

Progenitor cells in 8-20 weeks gestation arrested in prophase I, puberty start developing secondary oocyte arrested in metaphase of meiosis II after LH surge, complete at fertilization

40
Q

Sperm capacitation

A

Key event #1: freshly ejeculated sperm stripped of glycoproteins and seminal protein coat so can swim

41
Q

Acrosome reaction

A

Key event 2: Sperm recognize ZP3 which induced reaction, causes release of enzymes that break down the matrix and allows the sperm to penetrate reaction

42
Q

Gamete membrane fusion

A

Key event #3: The sperm and oocyte cell membranes fuse, start of fertilization, Ca2+ wave triggers completion of meiosis II

43
Q

The cortical reaction

A

Key event #4: Fusion triggers massive exocytosis of cortical granules which cross link ZP and degrade ZP3 blocking polyspermy

44
Q

End of fertilization

A

After pronuclei fuse, Cell undergoes S phase and is now ready to divide

45
Q

Spontaneous abortion rate

A

50%

46
Q

Major causes of early abortion (3)

A

Chromosomal abnormalities
Cleavage problems
Progesterone insufficiency

47
Q

PGE2 functions (3)

A
  • Contraction of thecal cells in ovulation
  • Blocks activation of both T-cells and NK cells after implantation
  • Stimulating the contraction of uterine myometrial cells during labor
48
Q

Types of uterine abnormalities (4)

A
  • Uterine fibroids
  • Congenital uterine development anomalies (Mayer-Rokitansky-Kuster-Hauser syndrome)
  • Excessive scar tissue (Asher an syndrome) May occur after uterine surgery
  • Excessive scar tissue from STIs (vaginal canal and cervix, not surgically treatable)
49
Q

Causes of low sperm number/function

A

HPT abnormalities

Varicocele

50
Q

Varicocele

A

A dilated testis vein the leads to the increase in temperature of scrotum, boiling sperm alive

51
Q

Aging (risk factor) (3)

A
  • Infertility
  • spontaneous miscarriage
  • Birth defects

Cell Biology (12 decks)

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