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HLTH 310 > HLTH 310 Test 3 > Flashcards

HLTH 310 Test 3 Flashcards

1
Q

The adrenal androgens stimulate the development of

A

pubic hair, armpit hair, body odor, acne

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2
Q

which is associated with an increase in secretion of DHEA and Adrenostenedione

A

Andrenarche

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3
Q

Which of the following events occurs EARLIEST in girls?
Question options:
breast budding
adrenarche
menarche
gonadarche

A

adrenarche

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4
Q

gonadarche

A

increased GnRH, increased gonadotropins, increased sex steroids, occurs during puberty and adulthood

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5
Q

what two important changes occur before puberty

A

decrease in sensitivity of hypothalamus and pituitary to negative feedback

increase in sensitivity of gonads to LH and FSH

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6
Q

What does LH and FSH trigger

A

testosterone production in testes and estrogen production in ovaries

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7
Q

what does the decrease in sensitivity of hypothalamus and pituitary to negative feedback cause

A

allows an increase in the production of testosterone and estrogen that stimulates the development of secondary sex characteristics

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8
Q

thelarche

A

breast budding, average age is 10-11, less than age of 8 is early, precocious

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9
Q

menarche

A

the first occurrence of menstruation, occurs 2-2.5 years after stage 3 tanner breast development. average age 11-12

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10
Q

average puberty for boys

A

average age is 12-13, younger than 9 is precocious, older than 14 is delayed

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11
Q

what are the effects of sex steroid hormones on growth

A

sex steroids increase GH secretion and sensitivity to GH.

Androgens directly stimulate longitudinal growth and muscle growth.

estrogens stimulate bone mineral deposition and osteoblast activity

estrogen mediates epiphyseal and metaphyseal fusion

androgens converted to estrogen by aromatase

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12
Q

pubertal growth spurt

A

it accounts for 20-30% of adult height and 50% of final adult peak bone mass

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13
Q

girls peak height velocity

A

9 cm a year at tanner stage 3, 12 years old

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14
Q

boys peak height velocity

A

10.3 cm a year at tanner stage 4, 14 years of age

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15
Q

what are the differences in final adult heights of male versus females due to

A

there is about a 13 cm difference, boys have 2 extra years of pre-pubertal growth, have a greater peak height velocity

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16
Q

who has an increase in muscle mass

A

males have greater muscle mass due to higher peak muscle growth velocity

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17
Q

who has more fat on their body

A

females have increased proportionate amount of fat in certain areas

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18
Q

who has wider hips

A

females have special cartilage in hips that respond more to estrogen

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19
Q

who has wider shoulders

A

males have special cartilage in shoulder joints that respond more to testosterone

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20
Q

lymph tissue growth

A

thymus, tonsils, lymph nodes regress after puberty

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21
Q

increased growth of what at puberty

A

reproductive tissues stimulated by sex hormones at puberty

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22
Q

CNS has a

A

continued growth, as well as changes in synapses, glial cell numbers, and myelination

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23
Q

growth of the heart

A

more or less isometric to body size

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24
Q

growth of brain

A

at birth your head is big compared to the rest of the body, then your body starts to grow and your head doesn’t look so big

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25
Q

proximodistal principle

A

first be able to control trunk muscles, then control arms, than fingers, than motor control of fingers

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26
Q

brain development timeline

A

cell birth, migration, axonal/dendritic outgrowth, programmed cell death, synaptic production, myelination, synaptic elimination/pruning

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27
Q

According to the McLean’s article called “Inside your teenager’s scary brain”, a long period of _____ growth in childhood, followed by vigorous ______ in adolescence, has been linked to higher intelligence
A.) white-matter; synaptic pruning
B.) grey-matter; synaptic pruning
C.) white-matter; synaptogenesis
D.) grey-matter; synaptogenesis

A

grey matter, synaptic pruning

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28
Q

grey matter

A

neuronal cell bodies and dendrites

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29
Q

white matter

A

bundles myelination axons that connect gray matter regions together

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30
Q

developing brain 4 years old

A

primary senses and basic motor skills are almost fully developed, vision has already matured

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31
Q

developing brain 6 years old

A

wernicke’s area language has development, brain has begun pruning process, prefrontal cortex has yet to develop, lack of reason, abstract thinking

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32
Q

developing brain 9 years old

A

basic motor skills are developed at age 5, burst of fine motor skill development between ages 8 and 9, parietal lobes beginning to mature, mathematics skills

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33
Q

standing with assistance age in months

A

4-9

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34
Q

standing without support age in months

A

5-11.5

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35
Q

hands and knees crawling age in months

A

5.5-13.5

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36
Q

walking with assistance age in months

A

6-14

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37
Q

standing alone age in months

A

7-18

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38
Q

walking alone age in months

A

9-18

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39
Q

critical period

A

child has heightened sensitivity to an external stimulus that is required for development of a skill, visual cortex

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40
Q

sensitive period

A

stages during development when development of a skill is easier due to greater sensitivity to an environment stimuli, language aquisition

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41
Q

developing brain 13 years old

A

prefrontal cortex last thing to mature, cant judge risks or make long term plans, emotion is controlled by prefrontal cortex but it is not mature yet so emotion is uncontrolled, logic is expanding as parietal lobes are growing rapidly at 13

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42
Q

developing brain 15 years old

A

not used connections in the brain will die, childs brain will become more specialized

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43
Q

developing brain 17 years old

A

maturing prefrontal cortex, burst of social interactions and emotions, planning, self control become more possible

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44
Q

developing brain 21 years old

A

brain appears to be almost fully developed, there needs to be development of emotional maturity, impulse control, and decision making still

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45
Q

What is a premature infant

A

an infant born before 38 weeks of estimated gestational age

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46
Q

low birth weight

A

under 2500 g 5lb and 8 oz

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47
Q

very low birth weight

A

under 1500g, 3lb 5oz

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48
Q

extremely low birth weight

A

under 1000g, 2lb 3oz

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49
Q

what is Barker hypothesis

A

inverse correlation between incidence of coronary heart disease and birth weight. lower birth weight higher risk for heart disease. associations are independent of lifestyle and occur in different populations mostly men levels of SES, smoking and alcohol use, obesity

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50
Q

the lower the birth weight

A

the higher the odds they had for impaired glucose intolerance

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51
Q

Barker hypothesis and programming

A

organs and metabolic/endocrine pathways are programmed during embryonic and fetal development according to environmental factors, this programming is long lasting and determines the set points of physiological and metabolic responses that continue into adulthood

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52
Q

programming will also include what with post-natal contributions

A

post-natal contributions, catch up growth may be involved and lifestyle factors interact as well

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53
Q

the mismatch hypothesis

A

According to the mismatch hypothesis, if the postnatal nutrition environment does not match the prenatal nutrition environment, the child will grow up to have a higher risk for development of hypertension, diabetes, obesity, disease later in life.

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54
Q

what happened to the pregnant rats fed low protein diet

A

offspring were born smaller, then catch up in growth
offspring have higher risk of obesity, high BP, hyperinsulinemia

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55
Q

chemical exposure during pregnancy

A

can increase risk of offspring obesity

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56
Q

what are the underlying mechanisms for fetal programming

A

hypothalamic-pituitary-adrenal axis and levels of stress hormone in the fetus
epigenetic modifications

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57
Q

deficiency in GH and/or IGF-1

A

short stature, as long as follow curve of growth no concerns, but if not follow growth curve then there is concern

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58
Q

treatment for GH deficiency

A

hGH, and rGH. still will be on lowest percentile even with medication but will follow the growth curve

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59
Q

Excess GH secretion

A

gigantism, acromegaly (growth of bones), usually due to benign tumors on the pituitary called adenomas

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60
Q

health issues with excess GH

A

joint pain, arthritis, osteoporosis
high blood pressure
heart failure from enlarged heart
compression of nerves leading to weakness, tingling in limbs, loss of vision, severe headaches
increased risk for diabetes mellitus
increased risk of colon cancer
sleep apnea

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61
Q

Laron syndrome

A

GH resistance
mutation in GHR or GH-induced intracellular signalling molecules
have high secretion of growth hormone, receptor not functioning, interfere with intracellular pathway
insensitive to growth hormone and low levels of IGF-1
small stature
lower risk of diabetes and cancer
Ghr-/- in mouse models

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62
Q

precocious puberty

A

puberty before age of 8 in girls and before age of 9 in boys
central causes traced back to hypothalamus or pituitary
peripheral causes are linked to sex steroids from abnormal sources
adrenal tumor
early puberty is more common in obese individuals

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63
Q

delayed puberty

A

hypogonadism- testis or ovaries produce very little or no sex hormone

hypogonadotropic hypogonadism- due to problem with pituitary gland or hypothalamus

causes- damage from surgery, injury, tumors, infections, high dose of glucocoticod meds, severe stress, rapid weight loss, kallmann syndrome is inherited form

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64
Q

genetic defects of hypogonadotropic hypogonadism

A

GnRH neuron migration, gnRH synthesis and release, GnRH action, gonadtropin synthesis

hypothalamus secret GnRH, pulses smaller, LH, FSH high amount

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65
Q

The type of study described in the Scientific American article called “Anguish of the abandoned child” about Romanian orphanages was a _________.
Question options:
randomized controlled trial
case-control study
qualitative study
cohort study

A

randomized controlled study

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66
Q

Which of the following statements, regarding the Scientific American article called “Anguish of the abandoned child” about the study on children in Romanian institutionalized care (e.g. orphanages), is FALSE?
Question options:
Children placed into foster care before age two had developmental quotients (DQ) that were ~10 points higher than children who were placed into foster care after the age of two.
Children placed into foster care before the age of two had EEG activity levels similar to children from the community who had never lived in an institution.
Children who had lived in an institution for any length of time had shorter telomeres than children from the community who had never lived in an institution.
Children placed into foster care had greater grey matter volume than children who remained in the orphanage.

A

Children placed into foster care had greater grey matter volume than children who remained in the orphanage.

(All institutionalized children had smaller brain volume. The foster care group has increased white matter volume but similar grey matter volume to the children who remained in the orphanage.)

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67
Q

In the Scientific American article called “Anguish of the abandoned child” about the study on children in Romanian institutionalized care (e.g. orphanages), all of the following outcomes were measured, EXCEPT
A) development quotient (DQ)
B) brain electrical activity (EEG)
C) ability to form attachments
D)telomere lengths
E)All of the above were measured

A

All of the above were measured

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68
Q

People with ____ are insensitive to growth hormone.
A.Achondroplasia
B.Laron syndrome
C.Acromegaly
D.Hypogonadotropic hypogonadism

A

laron syndrome

69
Q

Which brain system or area develops/matures the earliest?
A.Wernicke’s area
B.Limbic System
C.Primary somatosensory cortex
D.Parietal area

A

primary somatosensory cortex

70
Q

In gross motor development, the ability of an infant to control their trunk muscles and arms before they can control their hands and fingers is an example of the ________ principle of growth
A.cephalocaudal
B.proximodistal
C.allometric
D.accretionary

A

proximodistal

71
Q

cephalocaudal principle

A

humans grow from middle of body and out. direction of growth

72
Q

All of the following areas or functional systems of the brain are well-developed by age 13, EXCEPT
Question options:
limbic system
wernicke’s area
primary somatosensory cortex
primary visual cortex

A

limbic system

73
Q

senescence

A

decline in cellular function or viability called cell senescence

74
Q

aging is a complex process composed of what several features

A

an exponential increase in mortality with age

physiological changes that typically lead to functional decline with age

increased susceptibility to certain disease with age

75
Q

gerontology

A

the study of the aging process and individual as they grow from middle age through later life

study of physical, mental, and social changes

investigation of the changes in society resulting from our aging population

application of this knowledge to programs and policies

76
Q

geriatrics

A

the health care of older people including the study of health and disease later in life

77
Q

the median age is growing

A

1971 26.2 median age, 2011 39.9 median age, by 2060 25% of the population will be 65+

78
Q

life span

A

age at death for individuals

79
Q

maximum lifespan

A

theoretical limit on length of life for a species under ideal conditions

relatively fixed

80
Q

life expectancy

A

average numbers of years an individual can expect to live

highly variable

depends on many factors

81
Q

healthy life expectancy

A

average years of life in good health free from major disease, injury, or limitations on activity

82
Q

Canadian life expectancies

A

in 2017 LE of boys is 90.1 and females 92.5

1/2 of Canadians aged 20 today will reach 90

10% of those will reach 100

83
Q

why the dramatic increase in LE

A

better healthcare, better infrastructure, sanitation

84
Q

Top leading causes of death in 2020

A
  1. cancer
  2. heart disease
  3. COVID-19
85
Q

Top 5 leading causes of death in Canada by income

A

cancer is number one
heart disease
COVID-19
accidents
cerebrovascular diseases

all leading causes of death are higher among people from lower income

86
Q

chronological age

A

based on passage of time and not very useful for predicting someones level of health

87
Q

biological age

A

based on changes in the body that commonly occur with age

88
Q

primary aging

A

normal functional decline that is universal part of aging in the context of overall good health

normal mild cognitive decline and increase in forgetfulness

89
Q

secondary aging

A

declines due to hereditary defects and negative environmental influences

poor diet, lack of exercise, substance abuse, pollution, psychological stress

dementia

frailty, poor function of multiple organs/ systems

90
Q

genomic instability

A

damage to nuclear and mitochondrial DNA by free radicals, radiation, and mutagens, DNA mutation numbers increase with age

91
Q

telomere attrition

A

wearing down of the protective caps on chromosomes, telomeres shorten every time cell divides

92
Q

epigenetic alterations

A

modifications in gene expression, turning on aging genes and stopping young youthful genes leading to system wide loss of function

93
Q

loss of proteostasis

A

deregulation of the mechanics responsible for protein folding and recycling, leading to the accumulation of harmful by products

94
Q

deregulated nutrient sensing

A

loss of the cells nutrient level response, leading to impairments in energy production, cell growth, and other essential functions

95
Q

mitochondrial dysfunction

A

damage to mitochondrial DNA, resulting in reduced efficiency in energy production, increased oxidative stress, and the contamination of other mitochondria

96
Q

Cellular senescence

A

accumulation of senescent non-dividing cells in the body, impairing tissue function and increasing inflammation

97
Q

stem cell exhaustion

A

depletion of stem cell reserves, leading to a weaker immune system, and inadequate tissue repair

98
Q

altered intercellular communication

A

deregulation of the communication channels between cells, causing chronic inflammation and tissue damage

99
Q

AGEs

A

Advanced glycation end products

100
Q

what are AGEs

A

its a reaction between carbohydrates and free amino groups that create cross links

this increases stiffness in blood vessels, joints, bladder

impairs function in kidney, heart, retina

101
Q

epigenetic alterations

A

turns tissues into cellular mosaics

102
Q

aging gradual decline of whole systems

A

endocrine: estrogen (menopause), GH somatopause, Insulin resistance

immune system

103
Q

general concepts with aging

A

organ function depends on integrity of cells

most functions of organs remains adequate due to functional reserve with age

decline in one system/organ will affect others

older people most always have co-morbidities

104
Q

amount of active bone marrow decreases which causes

A

lower production of leukocytes needed for function of immune system

105
Q

how does the overall immune system slow down

A

innate immune declines, thymus regress making specific immune T-cells less effective, ability to make antibodies decreases

106
Q

aging immune system results in

A

increased vulnerability to infections

cancer is more common

vaccines less effective

slow wound healing

inflammation cause cause risk of other disease

107
Q

what happens to the heart as you age

A

increase in rigidity of heart

thickening of heart walls

heart fills with blood slower

maximum heart rate decreases

108
Q

what happens to blood vessels as you age

A

increase in thickness and stiffness

decrease in lumen (opening)

accumulation of plaques in arteries

109
Q

the result of an aging cardiovascular system

A

sometimes increase blood pressure

maximum heart rate decreases

reduced blood flow to cells and tissues

functions well under moderate activity but decrease in performance of athletes

slightly less tolerable to increased physical exertion or other stressors

110
Q

what is a cardiovascular disease with aging

A

atheroscerosis: fibrous plaques full of lipids, LDL particles, white blood cells, platelets, hypertension

111
Q

cardiovascular disease increased risk for

A

heart attack, stroke

112
Q

an early stage plaque is called

A

a fatty streak

113
Q

what happens in an aging respiratory system

A

stiffening of connective tissue in lungs

muscles of breathing weaken

number of alveoli and capillaries in lungs decrease

number and activity of cilia declines

weaker cough

114
Q

the result from aging respiratory system

A

decrease in maximum breathing

more difficult to expand lungs to full capacity

less able to clear mucus

less able to fight respiratory infections

115
Q

sarcopenia is

A

severe loss in muscle mass from disease or inactivity

116
Q

what happens to an aging muscular system

A

decrease in muscle mass, the fast twitch muscles, decrease in contractile force, normal is 10-15 decline, partially due to decrease in GH and testosterone, regular resistance training can delay loss in muscle mass

117
Q

aging muscular system results in

A

decreased motor performance in athletes

for sarcopenia increased fatigue and risk of falls

118
Q

if atrophy is due to disease

A

it is reversible

119
Q

if atrophy is due to sarcopenia

A

it is non-reversible

120
Q

what happens to bodies aging bones and joints

A

loss in bone density- reduction in thickness of compact bone, reduction in number and size of trabeculae spongey bone, osteoclast activity is more than osteoblast activity, menopause in women results in decrease estrogen which accelerates loss in women, loss in calcium

121
Q

where are bones most affected in loss

A

in the end of femur hip bone, at the wrists and spine vertebra

122
Q

osteoporosis

A

secondary aging process, more air spaces less trabeculae, more compressed osteoporotic vertebrae

123
Q

what happens to cartilage and ligaments as you age

A

cartilage that lines the joints gets thin and cracks, the ligaments and tendons stiffen and weaken

124
Q

what are the results of decline in bones and joints

A

increase risk of fracture, increased risk of tearing ligaments, stiffness, decrease in height, mobility problems, frailty in severe cases

125
Q

what are the changes in the endocrine system as you age

A

overall production of steroids and hormones decreases, changes in secretion of sex hormones

somatopause- steady decline in GH and IGF-1 levels with age

decrease in insulin sensitivity and in insulin secretion, glucose levels increase and it takes longer to recover

126
Q

type 2 diabetes

A

cells become resistant to insulin

over time beta cells cant keep up

this can lead to hyperglycaemia

high glucose levels damage tissues, blood vessels, and nerves

80-90% of people are overweight

increase risk for heart attack and strokes

127
Q

what is climacteric

A

fertility decline in men and women

128
Q

what is adropause in men

A

gradual decline in testosterone

minimal affect on fertility

129
Q

menopause in women

A

end of menstruation and reproductive capacity for women

early 50s

oocyte atresia- eventually no follicles left

first there is perimenopause

estrogen and progesterone decrease but LH and FSH increase

130
Q

consequences of estrogen loss

A

shrinkage of ovaries and uterus

vaginal tissue become thinner, drier, less elastic

breast tissue become less dense and firm

loss of estrogens ability to protect blood vessels, there is a decrease level of HDL

131
Q

what are normal declines in the brain and cognitive function with age

A

decrease in brain volume in certain regions

loss of white matter, myelination

increase in ventricle space

some loss of neurons

decrease in synaptic connections

arteries and blood vessels to the brain harden and shrink

decrease in certain neurotransmitter systems

these all lead to mild cognitive decline

132
Q

what is an abnormal change in nervous system

A

dementia, alzheimers

severe cell death and structural and biochemical abnormalities in brain leading to deterioration of mental and motor function

133
Q

risk factors for Alzheimers

A

age and genetics

family early onset, genes involved in 10 of cases

late onset gene is APOE4

environmental and lifestyle: atherosclerosis, high LDL cholesterol, diabetes, obesity, smoking, head injuries

134
Q

protective factors against Alzheimers

A

education, higher cognitive reserve

135
Q

Alzheimers pathology

A

increased inflammation and activated microglia

sometimes see evidence of infection

shrinkage of hippocampus, cerebral cortex, enlarged ventricles

136
Q

explain protein misfolding disease, whats involved

A

abnormal aggregation of tau protein inside neurons: neurofibrillary tangles

fibrils of beta-amyloid protein which come from APP: senile plaques outside neurons

137
Q

what happens to the inner ear as you age

A

age related hearing loss

loss of sensory receptors called hair cells

more loss in higher pitches, difficult to understand speech

vertigo or dizziness

tinnitus, ringing of ear

138
Q

what happens to eyes as they age

A

stiffening of lens

lens become denser

yellowing of lens

cell loss in retina and optic nerve

139
Q

what does aging of eyes result in

A

presbyopia

need for brighter light

changes in colour perception

140
Q

what are secondary disorders with eyes aging

A

cataracts

macular degeneration

glaucoma

141
Q

explain Weisman 1890

A

aging evolved to give advantage to species

142
Q

Peter Medawar 1950

A

accumulated mutation theory: aging results from accumulation of damage to somatic cells and genes for repair

143
Q

Williams 1957

A

antagonistic pleiotropy: genes that might improve chance of early survival can cause harm later on

144
Q

Kirkwood 1972

A

disposable soma theory

145
Q

Describe the disposable soma theory

A

evolutionary trade off between somatic maintenance and early growth and reproduction and natural selection

146
Q

lowering the activity of growth

A

increase maintenance and repair FOXO

147
Q

What is the role of FOXO

A

they are transcription factors that are mediators of insulin and IGF-1 signalling

in absence of insulin or growth factors they specify target genes

148
Q

FOXO in worm

A

daf-16

149
Q

FOXO in fly

A

dFOXO

150
Q

FOXO in mammals

A

FOXO 1,3,4,6

151
Q

An example of growth hormone resistance

A

Laron syndrome

mutation in GHR or GH-induced intracellular signalling molecules

less prone to type 2 diabetes and cancer due to lower IGF-A lower DNA damage and higher apoptosis as well as lower insulin

152
Q

Somatopause

A

steady decline in GH and IGF-1 levels with age

rGH has been looked at as an anti-aging therapeutic

a meta-analysis on the use of rGH only showed minor benefits

risks of this are cancer and type 2 diabetes

153
Q

reduced of what pathway increases lifespan

A

reduced insulin/ IGF-1 pathway

154
Q

Extra copy of what gene increases lifespan

A

Sir2 genes

155
Q

when what is inhibited increases lifespan

A

mTOR nutrient sensor

156
Q

longevity genes in centenarians, Barzilai and Ashkenazi Jewish

A

high correlation with high HDL and low LDL cholesterol levels

reduced activity in IGF1-R gene

157
Q

Longevity in Japanese and German

A

FOXO3A variants

158
Q

programmed theories of aging

A

biological clock programmed in our genes, turns down or shuts down genes at a certain time

epigenetic component

159
Q

damage-based/ stochastic theories of aging

A

wear and tear, damage due to assaults from both internal and external environments

failure of cellular repair mechanisms

160
Q

biological clock theory

A

gradual shutdown of nervous, endocrine, and or immune systems

triggered by genetic programs

clock in the DNA of the cell

161
Q

Telomeres and aging

A

repeated DNA sequences at ends of chromosomes that act as insulators

shorten with every cell division

can only be restored if telomerase is active

acceleration of telomere shortening is associated with certain diseases and unhealthy behaviours, as well as stress

162
Q

old versus new understanding of senescent cells

A

old was that they were good because they avoided becoming cancerous and bad because they promoted tissue aging

new is that they are bad because they promote cancer in other cells and secretions cause inflammation

163
Q

what are some assaults from internal and external environment that cause damage to the cell and its components

A

accumulation of waste

increased DNA breaks and mutations with age

free radical theory- damage from highly reactive molecules

misfolded proteins

cross-linking of DNA and proteins

decreased efficiency of repair mechanisms

164
Q

DNA damage theory

A

DNA mutations and chromosomal abnormalities increase with age

some progeroid syndromes are caused by mutations in genes related to DNA repair

165
Q

what are some attempts to slow aging

A

calorie restriction

sirtuin pathway- resveratrol activates

mTOR pathway- rapamycin inhibits

reactive oxygen species- neutralize with antioxidants and enzymes

blood transfusions and treatments to rebalance hematopoietic stem cell pool

166
Q

blood transfusions

A

no proven clinical benefit of transfusing plasma from young donors

older mice had signs of cell/tissue regeneration and higher cognitive and physical eprformance

167
Q

aged stem cells have

A

a myeloid bias, less lymphoid output thus decline in adaptive immune system, increased inflammation

168
Q

reasons for skepticism for ways to fix aging

A

yeast, worms, fruit flys, and mice are not humans

gains in lifespan with calorie restriction depend on strain and decrease with complexity of organisms, it can be dangerous for humans

genetic pathways found in model organisms involve multiple genes

rapamycin and other drugs can be dangerous for humans

conflicting evidence for ROS

cost and access to treatments create further inequities

HLTH 310 (1 decks)

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