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Growth week 4

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winniesmith2's version from 2017-10-30 21:31

Section 1

Question Answer
Who was David Barker 1938-2013first person to develop the idea that from birth we have the makeup that is our risk from non-commuincable disease. Due to maternal environment what the mother was exposed to at her child years.
What did barker and osmond do (1986)Looked at UK geographical distribution of mortality rates from CVD between 1968-1978 were closely related to infant mortality rates (a marker for poverty and low birth weight) from 1921 to 1925. C clear association between birth weight and eventual cause of death racket diabetes, cardiovascular disease)
What did barker et al state in 1989“…early environmental influences which impair growth and development lead to an increased risk for CVD in adulthood.
What did Osmond et al find in 1993The risk of CVD mortality birthweight <2500g (2.5kg) was double the risk >4000g. (4kg)
Describe standardised mortality ratios; UK men (barker et al 1989); data trendMortality ratio is low in people who had a larger birthweight.
what is standardised mortality ratio (SMR)A ratio percentage quantifying the increase or decrease in mortality of the study cohort with the spec to the general population. The ratio of observed deaths in the study group to expected deaths in the general population
What does it mean if SMR is quoted as a ratio and is equal to 1.0 then this means the number of observed deaths equals that of expected cases.
What does it mean if SMR is quoted as a ratio and is higher than 1.0 then there is a higher number of deaths than is expected. e.g. SMR = 1.04 for IHD in men with low birth weight then there are 4% more deaths in LBW group because of IHD than expected in the reference population
What does it mean if SMR is <1.0less people die than what is expected.
What is the fetal origins hypothesis (Barker 1995)“…fetal undernutrition in middle to late gestation…leads to disproportionate fetal growth, (which) programmes later coronary heart disease”
Flow from barker hypothesis to birth weightBarker hypothesis--> fatal programming --> predictive adaptive response--> low(er) birthweight (<2.5kg)
What happens to growth if babies are born with a low(er) birth weight exhibit rapid growth during infancy. Rapid growth (no constraints) sometimes called "catchup growth" (only if a constraint has been removed which then allows them to grow normally and 'catch up')
Describe catch-up growth>0.67 Z-scores from 0-2 years. 1 centile band difference between 2 centiles. 25th and 50th centile.
When is a classified rapid weight gainif z-score is 0.67
Normal weight gain V rapid weight gain at 0-2 years at 9 years. All people who showed rapid weight gain had lower birth weights than those of normal weights. The numbers were significantly different. lecture 2 page 65. Finally, catch up growth during infancy also demonstrates associations with later morbidity, notably obesity and type II diabetes (NIDDM)
Lower birthweight, rapid or catch up growth during infancy/childhood causes what which can lead to what diseasesIncreased height, weight, FM, FFM, central fat, insulin resistance, glucose intolerance. This leads to metabolic syndrome, obesity, type II diabetes, CVD.
Why do we have a childhood or juvenile growth spurtThe adrenal cortex develops and releases androgens cause a gross per/pubic hairs in girls
Look at graphspg 68-70
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Section 2

Question Answer
What is growththe formation of new tissue; increases in size and changes in shape caused by differential deposition of new tissue
What is the maturationthe process of the metamorphosis of the biological and chemical nature of tissue; the differentiation of cells, tissues, organs, and systems from dysfunctional immature states to functional mature states
How is growth assessedby measurement of specific dimensions (e.g. height, weight, etc.) using direct anthropometry, or imaging techniques (e.g. radiography, CAT, ultrasonography, radio-magnetic MRI, etc.) or indirect measures of body composition (densitometry, Body Impedance Analysis, volumetry, H2O or Air Displacement Plethysmography, etc.) !!!!! in comparison to a reference or standard .!!!!!!
How is my maturation assessedby functional assessment of specific organs and systems (e.g. cardiovascular, respiratory, reproductive, musculo-skeletal, etc.) using physiological tests of function (e.g. spirometry, sub-maximal and maximal stress testing, speed, endurance, balance, coordination, skill, etc.) against a reference or standard and assessment of maturity indicators in relation to full (adult) maturity (e.g. 2y sexual development, dental development, skeletal development, etc.)
How do we measure maturity-Not by height as it is variable. - Proportions change (shoulders/hip width). - Fat deposition. - Secondary sexual characteristics.
Maturity processes-Skeletal maturation -Dental maturation -Sexual maturation
Maturity events-Menarche -Spermarche -Voice change -Peak Height Velocity -95% adult height
What you have to consider when assessing maturity (six things)1. Maturity v Time 2. Discrete Maturity Indicators 3. Independence of maturational processes 4. Uneven maturation 5. Sexual dimorphism 6. Maturity v size
1. Maturity versus timeOne maturational year is not equal to one chronological year.
2. Discrete indicatorsMaturity indicators are discrete indicators of continuous processes
3. Independence of processesdifferent aspects of maturation are under different biological control
4. Uneven maturationNo two processes mature at the same rate
5. Sexual dimorphismMaturation rates differ between the sexes
6. Maturity v size a general but not specific relationship exists between size and maturity
Maturity indicator criteria (6)1. Universal (must occur in both sexes in all of them) 2. Sequential (must have a series of sequences of maturity to tell how mature it it) 3. Discrimination (demonstrate that two people of the same age can have different maturities) 4. Reliability 5. Validity (it is a real measure of maturity) 6. Completeness
Maturity indicated definitionA sequential and universal change in any part or parts of the body that is characteristic of the progression of the body from immaturity to maturity
memorize

Section 3

Question Answer
Tanner staging technique; -Breasts/Genitalia = B1/G1 – B5/G5 -Pubic Hair = PH1 - PH5 -Axillary Hair (arm pit) = AH1 - AH5
Pubertal stages; P1 (Pre- Pubertal)= B1/G1 + PH1 P2 (Pubertal ) = B2-B4/G2-G4 + PH2-PH4 P3 (Mature) = B5/G5 + PH5
Three questions to work out menarcheal age 1. Status quo: do you have (regular) periods? (Yes/No) 2. Prospective: have you started your periods since we last saw you? (Yes/No) 3. Retrospective (recall): When did you start having (regular) periods? (Age)
How much does menarche age varyRange 10-90%. Those with larger BMI tend to start earlier.
What does SFF stand forSpeaking fundamental frequency.
What is the SFF range of females165-255 Hz
What is the SFF range for males85-180 Hz
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Section 4

Question Answer
3 things to look for for skeletal maturation Primary ossification, Secondary ossification, Fusion.
Primary ossification: newbornLots of long/short bones to analyse. Cartilage becomes ossified
Compare hand skeletal growth at 12 yrs compared to 2.5yrsGrowth plates will disappear. Look at maturity with epiphysis and metaphysis/fusion of them.
What is the problem with measuring skeletal growth To measure, stage by stage, the metamorphosis of the cartilaginous and membranous skeleton of the foetus into the fully ossified bones of the adult. Membranous bone in head= allows for head moulding.
Skeletal maturity methodsNumber of ossification centres (related to genetics so not used). Planimetry (measuring area of bone). Atlas, bone-specific scoring - SURVIVED TECHNIQUES.
Bone specific scoring 0%= 0 maturity. 100%= full maturity. Identify markers along the way that relate to skeletal maturity. (Hand-wrist: Many bones, Different types, Changes from birth to maturity).
end of week 4 page 36
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