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FALL 2022 > PSIO 487 Exam 2 > Flashcards

PSIO 487 Exam 2 Flashcards

1
Q

Canities

A

hair graying

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2
Q

Hair

A

-Hair is made of dead, keratinized epithelial cells
-Hair follicle surrounds hair root
− Active telomerase
-Graying of axillary hair correlates very closely with age

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3
Q

The Integumentary System

A

Includes skin, hair, nails,
and sweat/oil glands
Functions:
− Protective barrier
− Contains sensory receptors
− Vitamin D production
− Temperature regulation

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4
Q

Layers of the Skin

A

Epidermis
Dermis
Hypodermis

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5
Q

Hypodermis

A

Mostly adipose tissue
− This is a subcutaneous
layer (not a part of the
integumentary system)

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6
Q

Dermis

A

− Connective tissue
− Contains hair follicles and
sweat glands

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7
Q

Epidermis

A

Epithelial tissue
Five layers of keratinized
stratified squamous epithelium

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8
Q

Keratinocytes produce

A

keratin
− Lipid-like secretion
− Toughens & waterproofs skin
− Like ‘mortar’ between cells
− Some telomerase activity in
keratinocytes

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9
Q

Melanocytes produce

A

melanin
− Involved in skin color
− Protects from UV exposure

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10
Q

The dermal-epidermal junction (DEJ)

A

− Anchors epidermis to dermis
− Interface for nutrient exchange and
signaling between layers

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11
Q

Connective tissue

A

Collagen provides tensile strength
− Elastin provides resilience

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12
Q

Biological Characterization of Aging Skin

A

§ Dullness, thinning, dryness, more visible pores, increased redness,
uneven pigmentation, dark spots, wrinkles, fine lines, tissue ptosis,
loss of elasticity

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13
Q

Intrinsic aging

A

naturally occurring aging of skin

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14
Q

Extrinsic aging

A

earlier deterioration of skin from exposure to
sunlight or pollution, lifestyle, etc

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15
Q

Collagen

A

− Provides structural network for support (tensile strength/firmness)
− Loss of collagen creates wrinkles and fragile skin
− With age collagenase activity increases, fibroblast synthesis of collagen
decreases

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16
Q

Elastin

A

− Provides stretch (resilience) and keeps skin pulled tight
− Loss of elastin function creates rigid, sagging skin
− With old age, elastin fibers develop crosslinks and become frayed/fragmented
− In some body regions, elastin network is thickened (but disorganized) with age`

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17
Q

Aging is associated with the appearance of

A

pseudoelastin

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18
Q

Wrinkles (intrinsic Factors)

A

result from changes in the connective tissue of the dermis

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19
Q

photoaging (extrinsic factors)

A

UV light exposure causes

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20
Q

Sweat Glands

A

− Eccrine: in most areas of body
− Apocrine: axillary region, genital area; this sweat produces odor if
broken down by bacteria

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21
Q

pheromones

A

axillary region, genital area; this sweat produces odor if
broken down by bacteria

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22
Q

Sebaceous glands (oil glands)

A

− Surround hair follicles
− Deposit sebum (oil) into hair follicles
* Nourishes hair, keeps from breaking

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23
Q

Nails

A
  • Slowed nail growth
  • Increased calcium deposition
    causes yellowing
  • Disappearance of the lunula
  • Appearance of longitudinal ridges
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24
Q

Cortisol

A

is a glucocorticoid hormone released by
the adrenal gland in response to stress
− Trauma, illness, exercise, cold, heat

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25
Q

Thymus

A

§ Small gland in mediastinum
§ Secretes thymosin à T cell maturation
§ Destroys autoreactive lymphocytes
− Negative selection (aka central tolerance)
− Peripheral tolerance also involved
(regulatory T-cells)

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26
Q

Thymic involution

A

− Begins shortly after birth
− Not induced by senescence (as once thought)

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27
Q

T Lymphocytes

A

Derived from bone marrow; mature in the thymus
§ High proliferative potential
− Long cellular lifespan (months-years)
§ Defense against intracellular pathogens
§ Help B cells generate an antibody response

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28
Q

T Lymphocytes from aged

A

Hyporesponsive T cells
− Reduced T cell diversity
− Lower production of new T cells
− Accumulation of senescent T cells
− Appearance of ‘hybrid’ T cell/natural killer cells

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29
Q

B Lymphocytes fro aged

A

− Decreased number of circulating B cells
− Reduced B cell diversity
− Lower production of memory B cells

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30
Q

B Lymphocytes

A

Derived from bone marrow; mature in the spleen
§ Important for antigen processing and presentation
§ Differentiation into plasma cells à antibody secretion

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31
Q

Immunosenescence

A

describes the complex changes that
occur with age and reduce immune system function

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32
Q

The Aged Immune System in aged

A

− Increased incidence of infections
− Increased incidence of cancer
− Decreased incidence of organ transplant rejection
− Decreased wound repair
− Increased incidence of autoimmune disease
− Increased tissue inflammatory disease (inflammaging)

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33
Q

Innate Immunity

A

− First line of defense; non-specific immunity
− Physical barriers (epithelial and mucosal linings)
− Macrophages, natural killer cells, and more

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34
Q

Adaptive Immunity

A

− Activated by innate immune response
− Reacts to specific pathogens
− Mediated by lymphocytes (T cells and B cells)

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35
Q

Allostasis

A

the process of restoring homeostasis with adaptive
responses to acute stressors
− “Maintaining stability through change”

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36
Q

allostatic load

A

(the effort required to maintain stability) can result
in damage over time
− Stress increases allostatic load

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37
Q

Stress-related inflammation has implications in many late-life diseases

A

Late-life depression and anxiety, cognitive decline, Alzheimer’s disease

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38
Q

Perceived stress

A

is strongly correlated with shortening of telomeres

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39
Q

Chronic stress

A

‘overrides’ negative
feedback signals to hypothalamus and
cortisol remains elevated
− Long-term suppression of immune system

40
Q

Hypothalamic-Pituitary-Adrenal (HPA) Axis

A

− CRH = corticotropin-releasing hormone
− ACTH = adrenocorticotropic hormone

41
Q

Menopause

A

the point in time when menstruation ceases as a
result of an age-related depletion of ovarian oocytes
begins with the final menstrual period (FMP)
− Median age of FMP is 51.4

42
Q

Perimenopause

A

begins with the first skipped or irregular period
− Median age of perimenopause onset is 47

43
Q

Male Hypogonadism

A
  • Low serum testosterone = below 200 ng/mL
  • Some symptoms may occur with 200-400 ng/mL serum T
    Symptoms
    − Fatigue/loss of energy
    − Low libido and erectile dysfunction
    − Reduced muscle mass
    − Increased fat mass
    − Osteoporosis
    -sometimes these symptoms are mistaken with lack of exercise
44
Q

Male HPG Axis

A

Hypothalamus - GnRH - anterior pituitary - 1. FSH - sertoli cells - inhibin (neg feedback to FSH through anterior pituitary) OR 2. LH - Leydig cells - testosterone

45
Q

Testosterone Replacement Therapy (TRT)

A

Monitoring of serum testosterone level is essential
Risks
− Prostate cancer
* SARMs
− Cardiovascular disease and/or cardiovascular events
Benefits
− Improve/maintain muscle mass and bone density
− Restore/maintain libido and erectile function
− Alleviate other symptoms of hypogonadism

  • it works for patients but not without risk (prostate cancer) do not increase the risk for prostate cancer or cause prostate cancer but if you have prostate cancer it will make it worse!
46
Q

Andropause

A

is an inaccurate term
− Androgen production and secretion does not cease
§ Androgen production and secretion DOES decline with age
− Symptoms are ‘real,’ but may be over-diagnosed and/or over-treated
as hypogonadism
− TRT is not always the answer

47
Q

The Menstrual Cycle

A

Day 0 = menses

Days 4-14
− Follicular phase (ovary)
− Proliferative phase (uterus)

Day 14 = ovulation

Days 14-28
− Luteal phase (ovary)
− Secretory phase (uterus)

48
Q

Cell Theory of Estrogen Production

A

FSH: acts on granulosa cells
to stimulate follicle growth and
estrogen production
LH: acts on theca cells to
stimulate androgen production;
LH surge triggers ovulation

49
Q

Granulosa cells
express

A

aromatase

50
Q

Estrogen levels rise
during

A

follicular phase

51
Q

Female HPG Axis

A

Hypothalamus - GnRH - anterior pituitary - 1. FSH = granulosa cells - inhibin (neg feedback for FSH) 2. LH = Theca cells - androgens

52
Q

neg feedback loop for female HGP Axis

A

Feedback loops between the
hypothalamus (GnRH),
pituitary (FSH & LH),
and ovary (inhibin and estrogen)

53
Q

The Macula

A

Located in the center of the
retina
NOT OPTIC DISC
-Responsible for central
vision (straight-ahead)
− Important for reading,
driving, recognition of
faces
-Highest concentration of
cone photoreceptors
− Color vision
− Less sensitive to light
than rod photoreceptors

54
Q

Damage to the macula

A

=macular degeneration = blurred central vision

55
Q

LH acts on

A

theca cells to
stimulate androgen production;
LH surge triggers ovulation

56
Q

FSH acts on

A

granulosa cells
to stimulate follicle growth and
estrogen production

57
Q

Granulosa cells
express

A

aromatase

58
Q

Estrogen levels rise

A

during follicular phase

59
Q

Retinal Pigment Epithelium (RPE)

A

Controls delivery of oxygen and nutrients to
the retina; also removes wastes

60
Q

Photoreceptors depend on

A

RPE for phagocytosis of outer segments
-a source of cellular debris

61
Q

Photoreceptors and RPE are subject

A

to chronic irradiation by visible light

62
Q

RPE sits on Bruch’s membrane

A

-Inner-most layer of the choroid
− Choriocapillaries are immediately deep to Bruch’s membrane

63
Q

Related Macular Degeneration (AMD)

A

is the leading cause of blindness in the US for people 55+
Risk factors:
− Age
− Race (Caucasian = higher risk)
− Smoking
− High cholesterol
− Genetics

64
Q

Dry (Non-Neovascular) AMD

A

Most common form of AMD

65
Q

Drusen

A

are deposited under the macula
− Drusen do not immediately cause
visual changes

66
Q

drusen can coalesce and cause

A

geographic atrophy of retinal pigment epithelium

67
Q

Wet (Neovascular) AMD

A

Invovles choroidal neovascularization (CNV)
− Blood vessels grow through macula after it is weakened by dry AMD
− Causes bleeding and scar tissue formation

68
Q

Pathogenesis of AMD

A

Abnormalities are observed in:
− Photoreceptors
− Retinal pigment epithelium
− Bruch’s membrane
− Choriocapillaries
-Dysregulation of RPE cell function is likely the most crucial event

69
Q

Treatment for Wet AMD

A

Susvimo: a port delivery system for anti-VEGF drugs
− Gene therapy

70
Q

innate immunity

A

-first line of defense , non specific immunity
-physical barriers
-macrophages, natural killer cells

71
Q

adaptive immunity

A

-activated by innate immune response
-reacts to specific pathogens
-medicated by B cells and T cells

72
Q

aged immune system

A

-increase infections
-increases cancer
-decrease wound repair
-increase autoimmune disease
-increases inflammatory disease (inflammaging)

73
Q

immunosenescence

A

describes the complex changes that occur with age and reduce immune system function

74
Q

B lymphocytes

A

-derived from twh bone marrow: ,mature in the spleen
-important for antigen processing and presentation
- differentiation into plasma cell for antibody secretion

75
Q

B cells in aged individuals

A

-decreases number of circulating B cells
-reduces B cell diversity
-lower production of memory B cells
-older can fight less pathogens than younger
-also worse at fighting past infections

76
Q

T lymphocytes

A

-derived from bone marrow: mature in the thymus
-high proliferative potential
-long cellular lifespan
-defense against intracellular pathogens
-help B cells generate an antibody response

77
Q

T cells in aged individuals

A

-hyporesponsive T cells
-reduced T cell diversity
-lower T cell production of new T cells
-accumulation of senescent T cells
-appearance of hybrid T cell/natural killer cells

78
Q

the thymus

A

-secretion of thymosin to mature T cells
-destroys autoreactive lymphocytes with negative selection (aka tolerance control)

79
Q

thymic involution

A

-begins shortly after birth
-not induced by senescence as once thought

80
Q

increase age with CVD

A

increased age is the greatest notifiable risk factor for CVD

81
Q

the prevalence of CVD

A

-increase with age
-lower prevalence of CVD in women before age 50 because of menopause
-estrogen is cardioprotective

82
Q

increase age for the heart

A

-left ventricular hypertrophy (mTOR, AMPK)
-diastolic dysfunction
-diminished cardiac reserve
-degeneration of the valve (mitral valve)
-cardiac fibrosis
-increase arterial stiffness
-loss of pacemaker cells (leads to resting heart decrease)

83
Q

cardiomyocytes and fibroblast with age

A

-large and flattened
-growth arrest
-telomere shortening
-SASP (senescence phenotype)

84
Q

atherosclerosis

A

-disease characterized by deposition of plaques (fat, cholesterol) on artery walls

85
Q

what does vascular aging contribute too

A

-inflammation of arterial vessel walls
-increase overall vascular diameter but narrowed lumen
-increase in fibrosis of intima layer

86
Q

estrogen favors what kind of fat distribution

A

-gynoid or pear shape
-menopause changes fat distribution

87
Q

lack of estrogen of cortisol favors what kind of fat distribution

A

-apple shape or android fat distribution
-increase risk for CVD and hypertension

88
Q

aging and the neurovascular unit

A

-pericyte (tight junctions) function decrease
-microglia (macrophages) number increase but function altered M1 ->M2
-cerebral endothelial cells have reduced NO production and impaired vasodilation

89
Q

Blood pressure with aging

A

-hypertension most common treatable risk factor in individuals with CVD

90
Q

What Happens in an Aging Brain?

A

§ Reduced brain volume in certain regions
§ Decreased number of neurons and
decreased speed of neurotransmission
− Oxidative stress, mitochondrial dysfunction,
and altered metabolism in neurons
§ Reduced blood flow to brain
§ Increased inflammation

91
Q

Perceptual Memory

A

§ Very short lasting (seconds)
§ Sensory memory
− Only stored momentarily in sensory
regions of the brain (e.g. occipital
lobe for visual stimulus)
§ Relies on primary sensory regions
§ The sensory areas that control
perceptual memory experience
little change with age

92
Q

Short-Term (Working) Memory

A

§ Information can be moved from perceptual
stores to working stores
§ Slightly longer (15-45 seconds)
§ Relies heavily on prefrontal cortex (PFC)
− PFC also important for concentration
§ Aging à short-term memory deficits
− Cell loss and shrinkage in PFC
− Reduced speed of neurotransmission
(especially pronounced in PFC)
NOTE: Older people are slower to reason
through decisions, but are better able to
make ‘gut decisions’

93
Q

Long-Term Memory

A

§ Requires learning of information
− Strategies: imagery, associations
§ Minutes to years
§ Relies on hippocampus
§ Requires storage and retrieval
§ Aging à long-term memory deficits
− Reduced activity, loss of cells, and
shrinkage in hippocampus
− Less cells = more overlap of information
between cells à interference/confusion

94
Q

Semantic Memory

A

§ Vocabulary & factual knowledge
− Lose details regarding time and
place of memory acquisition
§ Relies on temporal lobe
§ Mostly preserved with age

95
Q

Remote Memory

A

§ Memory from the distant past
§ Important for story-telling/‘folklore’
− Can include time and place that an
event occurred
§ Relies on temporal lobe
§ Typically preserved with age

96
Q

Normal cognitive aging

A

a gradual, age-related decline in memory,
conceptual reasoning, and cognitive processing speed

97
Q

Pathological Cognitive Decline

A

§ Dementia –- a condition characterized by a
decline in cognitive function that impairs an
individual’s ability to perform everyday tasks
§ Most common types of dementia:
1. Alzheimer’s Disease
2. Vascular Dementia
3. Lewy Body Dementia

FALL 2022 (5 decks)

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