L12 Chronic Diseases Flashcards

1
Q

what are the potential origins of western diseases

A

consequence of environmental changes accompanying industrialisation and prosperity

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2
Q

what are the two major environmental changes during industrialisation

A
  1. Hygiene
  2. Diet
    • - Improvements in sanitisation – fall in mortality rate form infective diseases (esp. children)
    • - Increased total calories, animal fat, fruit, fresh vegetables, vitamins, minerals – better growth and development (esp. children) and decline in infective diseases
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3
Q

childhood / early life factors of cardio vascular disease of T2D

A
  • Tended to grow slowly in utero (birthweights toward lower end of normal)
  • Tended to remain small for first 2yrs after birth and throughout infancy
  • After that, they gained weight and body mass index rapidly
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4
Q

Describe programming

A

Developmental plasticity

= adverse influences can permanently change body structure and function = ‘programming’

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5
Q

describe compensatory growth

A
    • If developmental growth falters due to malnutrition, it has ability - once adversity has ceased - to return to its growth trajectory by accelerated (compensatory) growth
    • If energy is allocated to rapid growth, allocation to some other developmental activity is reduced
    • In animals, compensatory growth has a wide range of physiological and metabolic costs that include premature death
    • costs of compensatory growth effects lifespan
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6
Q

what is size at birth due to

A

product of fetus’s trajectory of growth (set at early developmental stage) and maternoplacental capacity to supply sufficient nutrients to maintain this trajectory
• - Rapid trajectory of growth increases fetus’ demand for nutrients (greatest late in pregnancy)

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7
Q

link between placenta size and metal nutirtion

A

• - Depends on mother’s nutrition (diet, nutritional stores,
metabolism), which is the product of her lifetime’s nutrition (Jackson, 2000)
• - Depends on placenta’s ability to transport nutrients from mother to fetus (Harding, 2001), and is reflected in its size
• - Small babies generally have small placentas
• - Trajectory of fetal growth thought to increase with improvements in peri-conceptional nutrition

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8
Q

explain risk of male under development and placental condition

A
  • males placenta= less reserve capacity > increase vulnerability to under nutrition
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9
Q

what causes intrauterine growth restriction

A

developmental insult = placental changes (via poor nutrition) + maternal changes (execs corticoid exposure)

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10
Q

explain steps of developmental programming of obesity

A
  1. maternal exposures (substance abuse, poor nutrition, stress, smoking)
  2. developing fetes (growth restriction, increased fat storage)
  3. neonates (postnatal over nutrition, catch up growth, higher body weight)
  4. adult (phenotypic outcomes)
    metabolic syndromes= obesity
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11
Q

how can development of metabolic syndrome (post programming) be exacerbated

A

programmed physiology is challenged by excess nutritional load (e.g. high fat western diet) - underlying pathology may be exacerbated

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12
Q

glucocorticoid exposure =

A

decreased placental growth

+ HPA axis

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13
Q

developmental origins of CD

A

effect of intra-uterine or early postnatal development

• Many babies in utero receiving unbalanced and inadequate diets

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