HLTH 310 Test 3 Flashcards
1
Q
The adrenal androgens stimulate the development of
A
pubic hair, armpit hair, body odor, acne
2
Q
which is associated with an increase in secretion of DHEA and Adrenostenedione
A
Andrenarche
3
Q
Which of the following events occurs EARLIEST in girls?
Question options:
breast budding
adrenarche
menarche
gonadarche
A
adrenarche
4
Q
gonadarche
A
increased GnRH, increased gonadotropins, increased sex steroids, occurs during puberty and adulthood
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
6
Q
What does LH and FSH trigger
A
testosterone production in testes and estrogen production in ovaries
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
8
Q
thelarche
A
breast budding, average age is 10-11, less than age of 8 is early, precocious
9
Q
menarche
A
the first occurrence of menstruation, occurs 2-2.5 years after stage 3 tanner breast development. average age 11-12
10
Q
average puberty for boys
A
average age is 12-13, younger than 9 is precocious, older than 14 is delayed
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
12
Q
pubertal growth spurt
A
it accounts for 20-30% of adult height and 50% of final adult peak bone mass
13
Q
girls peak height velocity
A
9 cm a year at tanner stage 3, 12 years old
14
Q
boys peak height velocity
A
10.3 cm a year at tanner stage 4, 14 years of age
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
16
Q
who has an increase in muscle mass
A
males have greater muscle mass due to higher peak muscle growth velocity
17
Q
who has more fat on their body
A
females have increased proportionate amount of fat in certain areas
18
Q
who has wider hips
A
females have special cartilage in hips that respond more to estrogen
19
Q
who has wider shoulders
A
males have special cartilage in shoulder joints that respond more to testosterone
20
Q
lymph tissue growth
A
thymus, tonsils, lymph nodes regress after puberty
21
Q
increased growth of what at puberty
A
reproductive tissues stimulated by sex hormones at puberty
22
Q
CNS has a
A
continued growth, as well as changes in synapses, glial cell numbers, and myelination
23
Q
growth of the heart
A
more or less isometric to body size
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
25
proximodistal principle
first be able to control trunk muscles, then control arms, than fingers, than motor control of fingers
26
brain development timeline
cell birth, migration, axonal/dendritic outgrowth, programmed cell death, synaptic production, myelination, synaptic elimination/pruning
27
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
grey matter, synaptic pruning
28
grey matter
neuronal cell bodies and dendrites
29
white matter
bundles myelination axons that connect gray matter regions together
30
developing brain 4 years old
primary senses and basic motor skills are almost fully developed, vision has already matured
31
developing brain 6 years old
wernicke's area language has development, brain has begun pruning process, prefrontal cortex has yet to develop, lack of reason, abstract thinking
32
developing brain 9 years old
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
33
standing with assistance age in months
4-9
34
standing without support age in months
5-11.5
35
hands and knees crawling age in months
5.5-13.5
36
walking with assistance age in months
6-14
37
standing alone age in months
7-18
38
walking alone age in months
9-18
39
critical period
child has heightened sensitivity to an external stimulus that is required for development of a skill, visual cortex
40
sensitive period
stages during development when development of a skill is easier due to greater sensitivity to an environment stimuli, language aquisition
41
developing brain 13 years old
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
42
developing brain 15 years old
not used connections in the brain will die, childs brain will become more specialized
43
developing brain 17 years old
maturing prefrontal cortex, burst of social interactions and emotions, planning, self control become more possible
44
developing brain 21 years old
brain appears to be almost fully developed, there needs to be development of emotional maturity, impulse control, and decision making still
45
What is a premature infant
an infant born before 38 weeks of estimated gestational age
46
low birth weight
under 2500 g 5lb and 8 oz
47
very low birth weight
under 1500g, 3lb 5oz
48
extremely low birth weight
under 1000g, 2lb 3oz
49
what is Barker hypothesis
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
50
the lower the birth weight
the higher the odds they had for impaired glucose intolerance
51
Barker hypothesis and programming
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
52
programming will also include what with post-natal contributions
post-natal contributions, catch up growth may be involved and lifestyle factors interact as well
53
the mismatch hypothesis
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.
54
what happened to the pregnant rats fed low protein diet
offspring were born smaller, then catch up in growth
offspring have higher risk of obesity, high BP, hyperinsulinemia
55
chemical exposure during pregnancy
can increase risk of offspring obesity
56
what are the underlying mechanisms for fetal programming
hypothalamic-pituitary-adrenal axis and levels of stress hormone in the fetus
epigenetic modifications
57
deficiency in GH and/or IGF-1
short stature, as long as follow curve of growth no concerns, but if not follow growth curve then there is concern
58
treatment for GH deficiency
hGH, and rGH. still will be on lowest percentile even with medication but will follow the growth curve
59
Excess GH secretion
gigantism, acromegaly (growth of bones), usually due to benign tumors on the pituitary called adenomas
60
health issues with excess GH
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
61
Laron syndrome
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
62
precocious puberty
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
63
delayed puberty
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
64
genetic defects of hypogonadotropic hypogonadism
GnRH neuron migration, gnRH synthesis and release, GnRH action, gonadtropin synthesis
hypothalamus secret GnRH, pulses smaller, LH, FSH high amount
65
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
randomized controlled study
66
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.
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.)
67
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
All of the above were measured
68
People with ____ are insensitive to growth hormone.
A.Achondroplasia
B.Laron syndrome
C.Acromegaly
D.Hypogonadotropic hypogonadism
laron syndrome
69
Which brain system or area develops/matures the earliest?
A.Wernicke's area
B.Limbic System
C.Primary somatosensory cortex
D.Parietal area
primary somatosensory cortex
70
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
proximodistal
71
cephalocaudal principle
humans grow from middle of body and out. direction of growth
72
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
limbic system
73
senescence
decline in cellular function or viability called cell senescence
74
aging is a complex process composed of what several features
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
gerontology
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
geriatrics
the health care of older people including the study of health and disease later in life
77
the median age is growing
1971 26.2 median age, 2011 39.9 median age, by 2060 25% of the population will be 65+
78
life span
age at death for individuals
79
maximum lifespan
theoretical limit on length of life for a species under ideal conditions
relatively fixed
80
life expectancy
average numbers of years an individual can expect to live
highly variable
depends on many factors
81
healthy life expectancy
average years of life in good health free from major disease, injury, or limitations on activity
82
Canadian life expectancies
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
why the dramatic increase in LE
better healthcare, better infrastructure, sanitation
84
Top leading causes of death in 2020
1. cancer
2. heart disease
3. COVID-19
85
Top 5 leading causes of death in Canada by income
cancer is number one
heart disease
COVID-19
accidents
cerebrovascular diseases
all leading causes of death are higher among people from lower income
86
chronological age
based on passage of time and not very useful for predicting someones level of health
87
biological age
based on changes in the body that commonly occur with age
88
primary aging
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
secondary aging
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
genomic instability
damage to nuclear and mitochondrial DNA by free radicals, radiation, and mutagens, DNA mutation numbers increase with age
91
telomere attrition
wearing down of the protective caps on chromosomes, telomeres shorten every time cell divides
92
epigenetic alterations
modifications in gene expression, turning on aging genes and stopping young youthful genes leading to system wide loss of function
93
loss of proteostasis
deregulation of the mechanics responsible for protein folding and recycling, leading to the accumulation of harmful by products
94
deregulated nutrient sensing
loss of the cells nutrient level response, leading to impairments in energy production, cell growth, and other essential functions
95
mitochondrial dysfunction
damage to mitochondrial DNA, resulting in reduced efficiency in energy production, increased oxidative stress, and the contamination of other mitochondria
96
Cellular senescence
accumulation of senescent non-dividing cells in the body, impairing tissue function and increasing inflammation
97
stem cell exhaustion
depletion of stem cell reserves, leading to a weaker immune system, and inadequate tissue repair
98
altered intercellular communication
deregulation of the communication channels between cells, causing chronic inflammation and tissue damage
99
AGEs
Advanced glycation end products
100
what are AGEs
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
epigenetic alterations
turns tissues into cellular mosaics
102
aging gradual decline of whole systems
endocrine: estrogen (menopause), GH somatopause, Insulin resistance
immune system
103
general concepts with aging
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
amount of active bone marrow decreases which causes
lower production of leukocytes needed for function of immune system
105
how does the overall immune system slow down
innate immune declines, thymus regress making specific immune T-cells less effective, ability to make antibodies decreases
106
aging immune system results in
increased vulnerability to infections
cancer is more common
vaccines less effective
slow wound healing
inflammation cause cause risk of other disease
107
what happens to the heart as you age
increase in rigidity of heart
thickening of heart walls
heart fills with blood slower
maximum heart rate decreases
108
what happens to blood vessels as you age
increase in thickness and stiffness
decrease in lumen (opening)
accumulation of plaques in arteries
109
the result of an aging cardiovascular system
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
what is a cardiovascular disease with aging
atheroscerosis: fibrous plaques full of lipids, LDL particles, white blood cells, platelets, hypertension
111
cardiovascular disease increased risk for
heart attack, stroke
112
an early stage plaque is called
a fatty streak
113
what happens in an aging respiratory system
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
the result from aging respiratory system
decrease in maximum breathing
more difficult to expand lungs to full capacity
less able to clear mucus
less able to fight respiratory infections
115
sarcopenia is
severe loss in muscle mass from disease or inactivity
116
what happens to an aging muscular system
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
aging muscular system results in
decreased motor performance in athletes
for sarcopenia increased fatigue and risk of falls
118
if atrophy is due to disease
it is reversible
119
if atrophy is due to sarcopenia
it is non-reversible
120
what happens to bodies aging bones and joints
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
where are bones most affected in loss
in the end of femur hip bone, at the wrists and spine vertebra
122
osteoporosis
secondary aging process, more air spaces less trabeculae, more compressed osteoporotic vertebrae
123
what happens to cartilage and ligaments as you age
cartilage that lines the joints gets thin and cracks, the ligaments and tendons stiffen and weaken
124
what are the results of decline in bones and joints
increase risk of fracture, increased risk of tearing ligaments, stiffness, decrease in height, mobility problems, frailty in severe cases
125
what are the changes in the endocrine system as you age
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
type 2 diabetes
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
what is climacteric
fertility decline in men and women
128
what is adropause in men
gradual decline in testosterone
minimal affect on fertility
129
menopause in women
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
consequences of estrogen loss
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
what are normal declines in the brain and cognitive function with age
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
what is an abnormal change in nervous system
dementia, alzheimers
severe cell death and structural and biochemical abnormalities in brain leading to deterioration of mental and motor function
133
risk factors for Alzheimers
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
protective factors against Alzheimers
education, higher cognitive reserve
135
Alzheimers pathology
increased inflammation and activated microglia
sometimes see evidence of infection
shrinkage of hippocampus, cerebral cortex, enlarged ventricles
136
explain protein misfolding disease, whats involved
abnormal aggregation of tau protein inside neurons: neurofibrillary tangles
fibrils of beta-amyloid protein which come from APP: senile plaques outside neurons
137
what happens to the inner ear as you age
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
what happens to eyes as they age
stiffening of lens
lens become denser
yellowing of lens
cell loss in retina and optic nerve
139
what does aging of eyes result in
presbyopia
need for brighter light
changes in colour perception
140
what are secondary disorders with eyes aging
cataracts
macular degeneration
glaucoma
141
explain Weisman 1890
aging evolved to give advantage to species
142
Peter Medawar 1950
accumulated mutation theory: aging results from accumulation of damage to somatic cells and genes for repair
143
Williams 1957
antagonistic pleiotropy: genes that might improve chance of early survival can cause harm later on
144
Kirkwood 1972
disposable soma theory
145
Describe the disposable soma theory
evolutionary trade off between somatic maintenance and early growth and reproduction and natural selection
146
lowering the activity of growth
increase maintenance and repair FOXO
147
What is the role of FOXO
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
FOXO in worm
daf-16
149
FOXO in fly
dFOXO
150
FOXO in mammals
FOXO 1,3,4,6
151
An example of growth hormone resistance
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
Somatopause
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
reduced of what pathway increases lifespan
reduced insulin/ IGF-1 pathway
154
Extra copy of what gene increases lifespan
Sir2 genes
155
when what is inhibited increases lifespan
mTOR nutrient sensor
156
longevity genes in centenarians, Barzilai and Ashkenazi Jewish
high correlation with high HDL and low LDL cholesterol levels
reduced activity in IGF1-R gene
157
Longevity in Japanese and German
FOXO3A variants
158
programmed theories of aging
biological clock programmed in our genes, turns down or shuts down genes at a certain time
epigenetic component
159
damage-based/ stochastic theories of aging
wear and tear, damage due to assaults from both internal and external environments
failure of cellular repair mechanisms
160
biological clock theory
gradual shutdown of nervous, endocrine, and or immune systems
triggered by genetic programs
clock in the DNA of the cell
161
Telomeres and aging
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
old versus new understanding of senescent cells
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
what are some assaults from internal and external environment that cause damage to the cell and its components
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
DNA damage theory
DNA mutations and chromosomal abnormalities increase with age
some progeroid syndromes are caused by mutations in genes related to DNA repair
165
what are some attempts to slow aging
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
blood transfusions
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
aged stem cells have
a myeloid bias, less lymphoid output thus decline in adaptive immune system, increased inflammation
168
reasons for skepticism for ways to fix aging
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
