Aging – Biology and Pathology Flashcards

1
Q

The aging process tends to ___________ with advanced age.

A

accelerate (meaning you age more from 70 to 80 than from 20 to 30)

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2
Q

Discuss how the elderly population has grown in proportion to the total population over time.

A
  • 1900: 4% of the population was over 65
  • 2017: 13% of the population is over 65
  • By 2030: 20% of the population will be over 65
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3
Q

Women tend to live __________ longer than men.

A

7-10 years

Men tend to get more cancer and infectious disease.

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4
Q

The aging process affects every body system. For instance, ______________.

A

nerve conduction velocity decreases; GFR decreases; cardiac contractility decreases; lung vital capacity decreases

Note: fat does increase, though.

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5
Q

People tend to become ______-sighted with age.

A

far

Also called presbyopia

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6
Q

From age 35 to age 60, the brain ______________.

A

decreases by 10% mass

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7
Q

The kidneys shrink by ________________.

A

arteriolonephrosclerosis that leads to loss of nephrons

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8
Q

A normal adult kidney has about ___________ nephrons.

A

1,000,000

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9
Q

Most cancer deaths occur around age ___________.

A

70

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10
Q

What often causes subarachnoid hemorrhage?

A

Ruptured aneurysms

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11
Q

What are the two competing theories of aging?

A
  • Age is preprogrammed, like early development

* Age occurs due to oxidative stress (like rusting)

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12
Q

Which end of the DNA strand gets shortened in normal replication?

A

The 5’ end

This occurs because the RNA primer of the Okazaki fragment on the 5’ end of the replicated strand is removed by DNA polymerase I. This happens by 5’ to 3’ exonuclease activity. There is no 3’ to 5’ polymerase, so this end gets shortened.

Note: in all other Okazaki fragments, the upstream section will be filled in by DNA polymerase III and DNA ligase and thus not happen. In replicating the 3’ end, DNA polymerase III can replicate to the end, so this is only a problem for the 5’ end.

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13
Q

Why does telomerase add TTAGGG to the 3’ end of chromosomes?

A

This junk DNA is added to the 3’ end so that when the 5’ end gets shorter (as described in another card) that shortening does not eat into important genes.

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14
Q

What evidence supports the preprogrammed aging theory?

A
  • There are genetic disorders that lead to premature aging.
  • Stem cells and malignant cells can divide forever, but differentiated cells become senescent – stop responding to growth signals – after a finite number of divisions.
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15
Q

What evidence supports the oxidative theory of aging?

A
  • Mutations in metabolic genes that slow metabolism lead to longevity (e.g., defects in PI3K and IGFR lead to slowed metabolism and increased longevity).
  • Caloric restriction leads to longevity.
  • Older adults have a higher percentage of oxidized proteins than younger adults.
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16
Q

_____________ cells lack telomerase.

A

Somatic

17
Q

A lot of evidence has recently indicated that telomeres may set the biological clock. What research contradicts this?

A

Studies of families with telomere defects do not have early aging (though some have aplastic anemia and bone marrow failure).

18
Q

Werner syndrome results from a defect in ______________.

A

DNA helicase

19
Q

A new theory of aging posits that _________________ may play an important role in how we age.

A

mutations in mitochondrial DNA (which lack DNA repair enzymes and are subject to oxidative stress)

20
Q

What is lipofuscin?

A

Peroxidized lipids

21
Q

Subarachnoid hemorrhages and intracerebral hemorrhages are both types of _________________.

A

hemorrhagic stroke

22
Q

What causes progeria?

A

Defects in lamin A that lead to genomic instability

23
Q

Inhibition of ___________ slows metabolism and mimics calorie restriction.

A

mTOR (with rapamycin)