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HSS4102[A] > M1-Lecture 1 > Flashcards

M1-Lecture 1 Flashcards

Developmental plasticity and developmental programming, Identify critical windows, describe and identify common surrogates of the intrauterine environment, define mismatch, multiples hits.

1
Q

What does the DOHaD concept propose?

A

Environmental factors, especially during early life Deve. (prenatal and postnatal periods) can have lasting effects.

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2
Q

The mechanisms that mediate programming effects of environmental factors, or how memory is stored are unclear, but a few have been mentioned. T/F and list them

A

True
1. Excessive exposure to glucocorticoids (GCs)
2. Alteration in gene expression
3. Dysregulation of HPA axis.
4. Irreversible changes in organ structure.

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3
Q

How are we exposed to Glucocorticoids (GCs) exposure?

A

Either stress or medication

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4
Q

Cortisol’s role

A

Alters gene expression

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5
Q

Not having GCs receptors might predispose us to not be able to manage stressful situations? T/F

A

True

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6
Q

List some contributions to Chronic diseases?

A

Age
Smoking
Chronic Alcohol C.
Stress

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7
Q

Nutrition is the main one; however there are still other environmental influences? T/F

A

True

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8
Q

What was David Barker’s perspective on chronic diseases?

A

CD is more than bad genes and unhealthy adult lifestyle.

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9
Q

State David Barker’s hypothesis:

A

Exposure to environmental factors during critical/sensitive periods (prenatal and postnatal early periods), predispose us to diseases in adult life.

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10
Q

Low birth weight is a surrogate marker of the effects of prenatal environment on the fetus, and ‘fetal coping response” to that environment. T/f

A

True

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11
Q

David Barker’s observation to a theory. What does the theory state in brief?

A

Undernutrition during gestation linked to adult cardiac and metabolic disorders due to fetal programming that shaped body’s structure, function, and metabolism.

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12
Q

Ischaemic heart disease is not strongly correlated with both neonatal and postnatal mortality? T/F

A

False

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13
Q

Poor nutrition in early life (undernutrition - poor land, sparse food, urban poverty; and over-nutrition - rich land, abundant food, wealth, etc.)

A

Increases susceptibility to the effects of an affluent diet.

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14
Q

People living in parts with higher rates of neonatal death (sub-optimal pregnancy & early life experiences) lead to higher deaths from heart disease in middle and older ages? T/F

A

True

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15
Q

Environmental influences could impair growth and development in early life (prenatal and postnatal) leading to heart diseases, including Ischaemic HD in later life? T/F

A

True

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16
Q

Low-birth weight linked with insulin resistance, T2D, hypertension, & Dyslipidemia? T/F

A

True

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17
Q

Describe the relationship btw. LBW and HD.

A
  • Fetal programming (inadequate growth or suboptimal conditions in utero lead to developmental adaptations
    Ex: inadequate nutrition/stress (structural & functional changes)

This leads to:
CVS adjustment, metabolic adaptations (insulin resistance [for efficiency of nutrients], T2D, CVD). risk of hypertension, and more CvD, and chronic diseases.

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18
Q

What is SMR and used for?

A

Ratio btw. observed # of deaths and the deaths would expected based on age, sex and population size.

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19
Q

Studies have found that LBW increases mortality from CHD and too large birth weight as well? T/F

A

True

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20
Q

Boys and girls who would later get CHD had poor growth (LBW, were thin) from birth to age 2, after which their BMI increased. Including high BMI at 11 years compared to others. T/F and what it the term sued to refer to this?

A

True

Post-natal Catchup Growth

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21
Q

By how much does early exposure to famine increase CHD?

A

3x

22
Q

Early exposure to famine increases obesity (maybe normal weight at birth) in women?

A

true

23
Q

What is a characteristic of lighter/shorter at birth?

A

Mild exposure

24
Q

Mild exposure to Dutch Hunger cause obstruction of airways disease in adulthood?

A

True

25
Q

Late exposure characteristics (lighter, shorter at birth and throughout life), impaired glucose tolerance?

A

True

26
Q

Phenotypes can be induced in offspring without LBW?

A

True

27
Q

Reduction of fetal growth is not directly related to later disease.

A

True

LBW is a surrogate marker of fetal adaptation to adverse env

28
Q

FOAD vs DOHaD

A

FOAD studies intrauterine environmental exposures, affecting the fetus deve. during sensitive periods

DOHaD: exposure during critical plasticity period. prenatal and early postnatal.

29
Q

Btw. birth and age 5, 85% of brain’s wiring happens.

A

True

30
Q

ABILITY (not real manifestation) of an organism to develop in various ways in the particular environment or setting?

A

Developmental plasticity

31
Q

Developmental plasticity states that multiple phenotypes can arise during development of single genotype? T/F

A

True

32
Q

Different phenotypes are based on nature of the GxE interactions. T/F

A

True

33
Q

The range of phenotypes that can be induced in a given environment:

A

Reaction norm

34
Q

3 Characteristics of developmental plasticity:

A
  1. Nature of response dependant on nature of environmental cues.
  2. Critical windows - when system is vulnerable to change (or sensitive/susceptible to influences or disruptions)
  3. Duration is time limited: once organogenesis is complete (structure & function), plasticity is no longer (limited).
35
Q

Early heart - pulsating cells.

A

Yes

36
Q

See diagrams on

A

development plasticity

37
Q

What refers to whereby stimulus or insult, applied at “sensitive” or “critical” period of development, has lasting effects on the structure or function of the body. In other words, plasticity are expressed.

A

Deve. programming

38
Q

Deve. programming operates within context of plasticity. T/F

A

True

39
Q

Deve. programming leads to susceptibility to late diseases? T/F

A

True

40
Q

What is the purpose of deve. programming & dev. plasticity:

A

To allow organisms to adapt to their environment (fitness & survival)

41
Q

What model describes that organisms adjust their phenotype during development to avoid immediate death or impairment at expense of future health (trade-off)

A

Deve. constraints model (immediate adaptive response)

42
Q

Three points of predictive adaptive response (PAR) model:

A
  1. Organisms adjust their phenotypes based on cues during deve. to optimize their performance in future (predicted) environment.
  2. Fitness advantage when deve. environment matches predicted adult environment.
  3. May lead to disadva. when predicted environment is incorrect (mismatch).
43
Q

Not all environmental factors act through these plastic processes, disrupting rather adapting deve.? T/F - If True give example.

A

True (teratogenesis)

44
Q

Thrifty phenotype hypothesis:

A

Fetal adaptive response to promote survival in utero (can predict future environment) but it not may lead to developmental mismatch.

Trade-offs: altered anatomy & physiology - disease.

45
Q

Thrifty phenotype hypothesis examples:

A

Deve. constraints or PAR

46
Q

Three examples of contributing to evolutionary mismatch:

A
  1. Changes in our nutritional environment - appetite rewarding energy dense foods.
  2. Replacing human breast milk with cow’s milk- based formula.
  3. In vitro fertilization
47
Q

What happens when later life environment is different from that predicted in early life (maladaptation)?

A

Deve. mismatch

48
Q

Three contributing to examples to deve. mismatch:

A

Maternal illness
Placental disease
unbalanced maternal diet

  • These give false in utero cues

Significant changes in the post-natal environment.

49
Q

Thirfty Genotype example:

A

Repeated exposure famine led to + selection of efficient storage of energy.

Genetic polymorphisms that predispose individuals to obesity.

50
Q

Multiple hits steps

A

Prenatal life (first hit)

Early postnatal life (second hit)

Adult life (adult disease)

51
Q

Pathogenesis of disease is also determined by postnatal challenges. T/F

A

True

As well as early life exposures

52
Q
A

HSS4102[A] (13 decks)

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