Flashcards
K355 MT#2
Cards in this deck (118)
- 1Puberty definitionThe developmental process that culminates in reproductive capability & is results of complex series of molecular & physiological events
- 2Precocious puberty definitionWhen body changes/puberty happen earlier than normal
<8 for girls, 9 for boys
Average = 12-12.5 (girls), 11-14 (boys) - 3Tanner scaleMeasure of development via external primary & 2ndary sex characteristics
Girls: underarm hair, breast growth, hip growth, pubic hair, menstruation
Boys: facial hair, voice change, underarm hair, pubic hair, ejaculation
~80% reproducibility (Drs), self-report = over-estimate, 5 stages - 4Order of growthDistal before proximal
Ex. forearm before upper
Max growth in: tibia -> femur -> arms - 5Peak height velocityMax rate of growth/peak height during growth spurt
Indicator of somatic maturity
Max velocity of leg length, thigh/calf circumference before PVC - 6Timing of peak strength gainsBoys = 1.2 years after PHV
Girls = 0.6 years after PHV (more variable) - 7Timing of peak motor performance gainsStarts 1.5 years before PHV
Peaks 0.5-1.5 years after PHV - 8Timing of peak aerobic gainsAbsolute VO2 starts to increase several years after PHV but relative declines
- 9CSEP Guidelines 12-17At least 60 min of MVPA
Including: vigorous-intensity & muscle/bone strengthening 3+ days - 10Benefits of meeting PA guidelinesImprove health & fitness
Do better in school
Grow stronger
Have fun with friends
Feel happier
Maintain health body weight
Improve self-confidence
Learn new skills - 11Sedentary guidelines 12-17Minimize sedentary time
Limit rec screen time to 2 hours/day
Limit sedentary motorized transport, extended sitting & time spent indoors - 12Mechanisms of hormone actionsAutocrine - affects outside of releasing cell
Endocrine - released from gland, affects target after travelling through circulation
Intracrine - affects inside of releasing cell
Paracrine - affects neighbouring cell - 13Peptide vs. steroid hormonesPeptide = bind membrane receptor
Steroid = cross cell membrane to cause effect inside cell - 14What triggers body to start puberty?Don't know what starts the whole thing
-> hypothalamus releases gonadotropin-releasing hormone -> starts hormonal cascade -> gonadal activation -> puberty - 15Hypothalamus & pubertySecretion stimulated by specific neurons
Episodic bursts - freq & ampl vary between individuals & hormones
Feedback/regulation - circadian, environmental, etc - 16GnRHSecreted from hypothalamus
Stimulates secretion of LH & FSH from anterior pituitary - 17LH & FSH targetsMales: LH -> Leydig, FSH -> Steroli cells
Females: LH -> Theca, FSH -> Granulosa cells - 18LH & FSH in malesLH = interstitial/Leydig cells -> testosterone production -> spermatogenesis+
FSH = ABP/androgen binding protein -> sertoli/spermatogenic cells -> sperm - 19LH & FSH in femalesLH -> Theca folliculi -> androstenedione production -> estradiol
FSH -> Granulosa cells in ovaries -> production of sex steroids - 20Gonadotropin & menarcheGonadotropin increases in puberty for ~4 years, culminating with ovulation
Menarche = 1st period
(not regular for ~3 years) - 21Feedback loops in males1) Testosterone -> negative feedback on hypothalamus -> inhibits GnRH
2) Inhibin produced by sertoli cells when too many sperm -> negative feedback on GnRH - 22Female hormones pre-pubertyInhibin, progesterone, estrogen dampen GnRH release = prevents puberty
At puberty, hypothalamus become less sensitive to this inhibition - 23Female cyclesOvarian = Follicular phase (primary, 2ndary, vesicular follicle), Ovulation (from rise in LH), Luteal phase (formation of CL, until pregnancy/CL degradation -> progesterone decr)
Uterine = Menstrual (1-5), Proliferative, Secretory - 24Hormone peaks in female cycleLH & FSH = at ovulation
Estrogen = spike at ovulation, drops, then slight hill, drops again
Progesterone = low until CL formation, parabola - 25GnRH throughout lifeChildhood = low
Puberty = higher & pulsatile at night
Reproductive years = higher & pulsatile
Menopause = very high & pulsatile - 26Determinants of GnRHMuch unknown
Growth factors
Nutrition (critical fat hypothesis)
Genetics
Maybe ethnicity, obesity, epigenetics - 27Nutrition & puberty linksChronic malnutrition/malabsoprtion diseases -> delyaed puberty
Link between amount of fat/leptin & onset of puberty - leptin affects GnRH+ - 28Connections of adipocytesConnected by collagen networks
Neural connections & rich blood supply - 29Stages of adipose differentiation & markersStem cells -> Adipoblasts
-> Preadipocytes (LPL, fat)
-> Very small adipocytes (LPL, fat, IGF-1)
-> Mature adipocytes (LPL, fat, IGF-1, TNF-α. AGT, PAI-1, HSL, FABP) - 30Fat cell developmentMost fat cells are formed during embryogenesis
Derived from mesenchymal stem cells
Pre-adipocytes = fatty acid translocase, LPL
Very small adipocytes = small lipid droplets - 31Factors influencing fat cell size & numberSize: + = excess insulin & cortisol, testesterone & GH deficiency
- = excess GH & TH
Number: + = excess insulin, cortisol, GH, TH
- = GH & TH deficiency - 32White vs brown fatWHITE: large, singular, abundant, few simple mitochondria, for storage, located everywhere
BROWN: smaller, many droplets, <1%, many connected complex mitochondria, for heat, distinct locations - 33Why babies need brown fatLess skeletal m.
Reluctance/inability to shiver
Dec/slow NS response to cold
Can't move away from cold
Huge hairless heads
Large SA:mass ratio - 34UCP1In brown fat
Uncoupling protein
Dissipates normal proton gradient to make ATP -> make heat instead - 35Brown fat decreases with...Higher outdoor temperature
Higher BMI
Increasing age
M < W
Diabetic < normal - 36Prenatal fatNot until ~14 weeks gestation, mostly abdominal
Increased number & vascularization of adipocytes at 23 weeks
Small cells
Needed for energy after birth (stress!) - 37Postnatal fat info5-50 billion adipocytes in young adult
Diameter grows from 30 um -> 100 um
Volume = 0.5-10 kg (males), 14 kg (females)
Size varies by location - 38Fat metabolism/storage (white)LPL hydrolyzes FFA from lipoproteins
-> FFA enter adipocytes
-> TG -> fat droplet
Hormone-sensitive lipase -> hydrolysis of TG to FFA -> circulation
Lipolysis = higher in kids (higher sensitivity to catecholamines) - 39Fat accumulation during growthBoys: pre-adolescent fat wave @ ~12
Girls: steady increase after ~8
Obese kids >6yo = greater risk of adult obesity (not absolute) - 40Overweight/obesity rates in Canada59% of adults
26% of kids = tripled in last 25 years
Costs = $4.3 billion - 41Waist circumference cut offsMen = 102 cm
Women = 88 cm - 42Fat changes with obesityIncr adipocyte volume 2-3x
Decr beta-receptor response (lipolysis)
Decr insulin sensitivity
Incr lipids & BP - 43Cuba's natural experiment1989-2000 economic crisis -> decr nrg intake, incr PA -> population weight loss
Decline in deaths due to: diabetes (51%), CHD (35%), stroke (20%), all cause (18%) - 44Types of bone cellsOSTEOGENIC cell = stem cell
OSTEOBLAST = bone deposition/growth, secretes factors hardening into bone
OSTEOCYTE = mature bone cell, maintain bone matrix, star-shape, sensors, 1/2 life = 25 years
OSTEOCLAST = bone resorption/ remodeling, 5 nuclei, suction cup -> re-absorptive pit, digestive enzymes - 45Cycle of bone remodellingResorption -> Reversal Phase -> Formation -> Resting Phase
Childhood = mostly formation
Adulthood = equilibrium (mostly resting)
Old age = mostly resorption - 46Where does endochondral ossification occur?In long bones
- 47Endochondral ossification process1) Bone collar around hyaline cartilage (week 9)
2) Bone collar growth, cartilage in diaphysis calcifies, cavities form
3) Periosteal bud invades cavities, spongy bone starts to form (month 3)
4) Diaphysis elongates, medullary cavity forms, ossification, 2ndary ossificaiton centers form in epiphyses (birth)
5) Epiphyses ossify, hyaline cartilage only left in epiphyseal plates & articular cartilage (childhood-adolescence)
Growth plates fuse @ 18/21 - 48Zone of endochondral ossification growthProliferation zone: mitosis in cartilage cells
Hypertrophic zone: older cells enlarge
Calcification zone: matrix calcifies, cartilage dies, matrix starts deteriorating
Ossification zone: new bone formation - 49Growth plate fracturesMost common injury in kids
But also quicker healing (3 wks in infant, 8 wks at 8 wks, 20 wks at 20 yrs)
But more risk of complications - growth disturbances, PT myositis ossificans - 50Where does intramembranous ossification occur?In other (non-long) bones - ex. skull
- 51Intramembranous ossification process1) Ossification centers appear in fibrous connective tissue membrane (via OBs)
2) Bone matrix/osteoid secreted from OBs in membrane & calcifies, trapped OBs -> OCys
3) Woven bone (of trabeculae) & periosteum (vascularized) form
4) Lamellar bone replaces woven bone (deep to periosteum) to form compact bone plates, vascular tissue of spongy bone (deep) becomes red marrow - 52How to measure bone?DEXA
- 53Female Athlete TriadMenstrual dysfunction + Osteoporosis + Disordered eating/low energy availability
2-4x more stress fractures, low body temp, high cortisol, low T3/T4, low IGF-1, low BMR - 54Menstrual classificationsEumenorrheara = normal
Oligomenorrhea = infrequent, light, irregular, >35 day cycle
Amenorrhea = 3+ missed cycles, 1st degree = never started, 2nd degree = started & ceased (ex. pregnancy) - 55Skeletal age in athletesThroughout development, difference bt skeletal age & chronological age = positive in athletes/greater than non-athletes
-> athletes = bigger
Via selection or effect of sport? - 56Optimal window for bone densityBefore/at puberty = optimal time to increase bone density
Ex. look at R/L differences in squash players - largest differences in players starting before/at puberty - 57Age at menarcheMean = 13 y
95% between 11-15
More athletes later - 58Relation between menstrual dysfunction & ...BMD = Negative relation
Weekly distance run = Positive relation - 59Features of DMDProgressive m. weakness,
In wheelchair by early teens
Eventually affects respiratory m.s
Death in late teens/early 20s
X-linked recessive condition (males affected, females carry)
1/3000 - 60Cause of DMDDeletion/mutation of part of dystrophin gene -> loss of sarcolemmal integrity -> m. fibers more susceptible to damage
B/c dystrophin = link bt intracellular cytoskeleton & extracellular matrix = mechanical stress resistance - 61Gower's signClassic sign of DMD
Due to proximal m. weakness
Unable to stand normally, climb up themselves - 62Treatment of DMDNo cure
Physical therapy & orthopedic appliances
Oral prednisone (side effects!) - 63Muscle structure
- 64Embryo germ layersGastrulation: germ layer formation, 3wks
ECTODERM = outer - skin, nerve tissue
MESODERM = middle - m, bone, connective tissue, heart, kidneys, etc
ENDODERM = inner - epithelial lining (lungs, stomach, glands, urogenital tract) - 65Skeletal muscle differentiation processEmbryonic mesoderm cells -> cell division & enlarge -> myoblasts -> fuse -> myotube -> matures -> skeletal m. fiber
- 66Satellite cellsFor regenerative capacity of skeletal m. - provide MBs for growth then become dormant until needed for more MBs
Active in growth & development
Located b/t basal lamina & sarcolemma
Tiny, discovered in 1961
Skeletal m. doesn't regenerate w/o them
Classified as stem cell - 67Regenerative capacity of muscle typesSkeletal = limited
Cardiac = limited
Smooth = regenerate throughout life - 68Muscle/coordination developmentHead -> toe
Proximal -> distal
Muscular development reflects nm. coordination
Peak natural neural control ~midadolescence - 69% muscle mass males vs. femalesFemale = 36%
Male = 42% (testosterone)
Strength/unit = same - 70Muscle fiber diameter males vs femalesSame until adolescence
then males > females - 71Muscle fiber differentiationMostly undifferentiated <30 weeks
Type 1 & 2 appear ~30 weeks
1 = 40% at term
2 = 45% at term
Growth -> varying % bt individuals - 72Prenatal skeletal muscle development summaryMostly Hyperplasia, some hypertrophy
Gastrulation (germ layers) = incr. # + size
-> embryonic mesoderm -> incr. # + size
-> myoblasts -> myotubes -> small fibers
Coordinated gene expr. + epigenetics
Positive & negative regulators
ATP = 0.5 mmol/kg
Lower nitrogen - 73Postnatal skeletal muscle development summaryEarly hyperplasia -> mainly hypertrophy
# fibers doubles in 1st 4 months
Continued incr in #, L & size + remod.
Satellite cells (can incr myonuclei #)
ATP = 3 mmol/kg
Increase in nitrogen, mito, & oxidative + glycolytic enzymes - 74Child/adult skeletal muscle development summaryIncr d & L of existing fibers (d doesn't change after adolescence)
Satellite cells
M. loss starts ~30y
ATP = 5 mmol/kg
Increase in nitrogen/protein
Epigenetic influences; +/- regulators - 75Heart development in uteroCells in embryonic disk fuse to form primitive heart @ 3 weeks
Beats shortly after
Grows into pericardial cavity - 76Heart development in utero pic
- 77Congenital HD1% of live births
Most freq congenital malformation in babies
Causes: measles, alcohol, etc
Septal defects, stenosis, patent ductus arteriosus, artery transposition - 78Vascular shuntsShould all close at birth
1) Foremen ovale
2) Ductus arteriosus
3) Ductus venosus
Closed by change in pressure at birth - incr. BP & decr pulmonary resistance - 79Foremen ovale1-way opening in septum b/t atria (R->L)
Allows bypassing of fetal lungs
1st shunt
Closes at birth - 80Ductus arteriosusBypass directly into aorta to divert blood from lungs (outside heart)
Only 10-15% of blood gets to lungs in fetus
Closes at birth - 81Ductus venosusUmbilical cord to inferior vena cava to RA
Bypasses the liver
Closes w/i 1st 3 days of birth - 82Ventricle & heart sizeRV = LV at birth -> shaped by pressure & resistance
Heart mass, size & volume incr with age
But volume : BW ratio = mostly constant - 83Changes in heart rateBirth = 140 bpm
1yo = 100 bpm
6yo = 80 bpm
10yo = 70 bpm
Sex differences @ puberty -> males = 5 bpm lower (57-60)
Decreased respiratory rate with age - 84RBCs, Hb & hematocrit levelsRBCs: puberty -> big incr only in boys
Hb: incr in pre-puberty, extra spike in boys @ ~14
Hematocrit: 50% at birth, drops to 30% @ 2, increases again to 45/40% (M/F) - 85Prenatal lung developmentSingle pound @ 4 wks
Early differentiation @ 16 wks
Alveoli develop @ 3 months
Lungs are filled with fluid & blood - most expelled during birth or during lymph - 86Cardiorespiratory changes at birthHuge drop in pulmonary resistance
Huge incr in pulmonary blood flow
Decr in pulmonary arterial pressure
1st breath = hardest (pulmonary P)
Ventilatory effort opens alveoli
Breathing also promoted by tactile stim, decr skin temp - 87Number of alveoli20 mill @ birth
300 mill @ 8 years - 88SurfactantReduces surface tension of alveoli
Lipoprotein
Produced in last 2 months of utero - 893 approaches to talentSelection = athletes already competing selected for extra opportunities
Detection = introduction of new talent with certain skills
Transfer = existing high perf athletes targeted for a diff sport - 90AsthmaShortness of breath, wheezing, coughing
Caused by inflammation of respiratory airways &/or excessive contraction of airway muscle
Exercise-induced = main reason for sedentary lifestyle
Normal fitness unless severe - 91Cerebral palsyMost common nm pediatric disease (2/1000)
Caused by damage to motor control centers of brain
70-80% of patients = spastic = loss of mn inhibition -> excessive m. contraction
Among least active w/ CCC, low VO2max - lack of coordination/strength - 92Cystic fibrosisA genetic disorder affecting lung, pancreas & other organs
No cure
Mutant CFTR doesn't move Cl -> sticky mucus outside cell
Usually as active until progression (decline in aerobic capacity b/c impaired lung fxn) - 93Type 1 diabetes mellitusInsulin dependent diabetes
Pancreatic beta cells destroyed by immune system
No apparent cause
Insulin therapy - 94Extremely low birth weight<1000 g
Caused to preterm birth or slow prenatal growth rate
Short height, in childhood, no change in maturation - 95Concepts of motor developmentElongation -> activation
Flexion -> extension
Cephalic -> caudal
Asymmetry -> symmetry
Gross -> fine - 96Motor development - ElongationFirst m.s to develop = back extensors
Then frontal elongation
Then sitting - 97Motor development - Cephalic to caudalOrder of myelination & synaptic development
Hands -> feet
Neck -> low back -> pelvis - 98Motor development - symmetry1st movements are asymmetric
Symmetry should start by month 4 - sign of neurological delay - 99Primitive reflexesAsymmetric tonic neck reflex
Moro
Rooting
Grasp - 100Asymmetric tonic neck reflex- Arm extends toward head tilt
- Movement through birth canal, hand-eye
- Lack of integration -> can't turn over, poor posture & visual perception, awareness issues
Till 4 months - 101Morro reflexStimulated by sudden change in position
For flight/fight, sensing enviro
Poor integration -> chronic fatigue from stress hormones, hypersensitive, impulsive
Till 2-4 months - 102Rooting reflexTouch of face -> open mouth, searching w/ lips & tongue = searching for food
Disappears at 4 months when vision/hands take over to find food - 103Grasp reflexFor clinging to mom, from touching hand
Till 3 months
Delay = indicative of neural development delay/injury
Learn to let go, not to hold - 104Developmental reflexesTonic labyrinth righting reflex
Optical righting reflex
Landau
Start ~3 months - 105Tonic labyrinth righting reflexIf head bends fwd -> body flexes
If hand bends back -> body extends
Poor integration -> bad balance system, head flops fwd, poor posture/learning position, dyspraxia/poor coordination, motion sickness - 106Optic righting reflexEye position will signal to right head/neck/ body, attempting to keep eye level
- 107LandauProne position in air -> extension of head & hips & knee flexion - help development of lumbar curves (shock abs) & head control
Abnormal landau = hypotonia or hypertonia - 108Point of weightAt birth = at cheeks
-> Shoulders @ 2 months
-> Belly/thorax @ 4 months
-> Hips - 109Sitting in developmentTripod sitting @ 4 hands
Bum supporting weight @ 5 months
Trunk control @ 6 months
Lordosis while sitting, moving in/out @ 7 months - 110Mobility milestonesRolling @ 4 months
Crawling @ 6-7 months
Bear walking @ 6-7 months
Scooting @ 6-7 months (shoudn't be only!) - 111Standing developmentPulls to standing @ 5 months
Takes full weight standing @ 6 months
Move from stand to various position @ 8 months - 112Walking milestonesStep gait/hands held (legs abd, + ext rot) @ 8 months
Lower extremity striding, pelvic rotation @ 9 months
Cruising around furniture @ 11 months
Unassisted walking @ 12 months - 113TorticollisShortening of sternocleidomastoid -> head tilts to affected side, look other way
Causes: birth trauma, lack of interuterine space, low amniotic fluid
Treatment: exer, brace - 114PlagiocephalyFlat/misshapen head due to repeated pressure on same side
Compounded by torticollis, premature, back to sleep program
Treatment: counter position, tummy time, helmets - 115Toe walkingCauses: short Achilles, exersaucers, autism, social factors
Treatments: exer program, ankle/foot mobilization, prism lenses, bracing, serial casting, surgery - 116Hip dysplasia & dislocationShallow acetabulum/lax ligaments
Unknown cause, familial, increased by breach position in utero, cultural factors
S/S: hip click, asymmetric buttcrack, issues diapering/limited ROM abd + flex, pain (childhood), exaggerated sway back
Treatment: Pavlik harness, cast, surgery - 117W sittingDevelopment usually via external factors
Incr hip dislocations, esp with hip dysplasia
Can't reach across body - delays hand dom
Can't laterally shift weight - trunk m. development delayed - 118Red flags in babiesSnorting/snoring
Colic (vagus n.)
Car seat crying (myofascial damage)
Interrupted sleeping
Can't suck soother/nurse (hypoglossal n)
Crying on back
Irregular bowel movements
Scars
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- Flashcards on K355 MT#2, created by Megan Willerth on 04/03/2015.
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