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RDA > Adolescence and puberty > Flashcards

Adolescence and puberty Flashcards

1
Q

What is meant by adolescence

A

• Adolescence – phase between childhood & adulthood • Pubertal development may be start of adolescence

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2
Q

What is meant by adulthood

A

• Adulthood: legally, culturally variable • UN: children < 18 years

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3
Q

What is the current age of adolescents and what is it expected to be soon

A

Current : 10-20

Future : 10-25

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4
Q

Summarise the cognitive/ emotional changes that take place during adolescence

A

 Emotional change  Reasoning - more abstract  Greater knowledge / awareness of world  Identity – of self, family, ethnicit

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5
Q

Summarise the changes in family relationships that take place during adolescence

A

Challenging rules  Discipline needs reasoning  Less confiding & intimacy in parents

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6
Q

Describe the changes in peer relationships that take place during adolescence

A

 Peer activities / confiding  Sexual relationships  Peer group influences values and behaviour (pro / anti -social

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7
Q

Summarise the biological changes that take place during adolescence

A

• Puberty / Endocrine changes secondary sexual characteristics • Physical growth

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8
Q

What are the different developmental changes that occur during adolescence

A

§ Developmental stages of adolescence:
o Early 11-14.
o Middle 14-17.
o Late 18-21.

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9
Q

Describe adrenarche

A

• Starts: • Females: 6-9 years • Males: 7-10 years • Rise in adrenal 19- carbon steroid production, dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS). • Manifests clinically as the appearance of axillary and pubic hair, usually about age 8. • Role uncertain -?Precursor to puberty

Soley dependent on adrenal androgens

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10
Q

Summarise the physical development that takes place during puberty

A

§ Physical development:
o Gender differences – girls grow taller, start puberty and are more mature, earlier than boys do.
o Pubertal changes – girls start puberty around 8 (with breast budding) whilst boys start around 10.5.
§ Peak for girls is 11-13.5, peak for boys is 13-15.
§ Early maturing girls and late maturing boys are at risk of – depression, substance abuse, ASBOs, eating disorders and bullying.

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11
Q

Define puberty

A

Puberty: growth due to synergy of gonadal steroids and growth hormone (APG)

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12
Q

What is growth due to in puberty

A

Is due to the GONADAL STEROIDS (particularly ANDROGENS) working in conjunction with other hormones, particularly
SOMATOTROPHIN (Growth Hormone) from the adenohypophysis

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13
Q

What are the two theories regarding the onset of puberty

A

§ Onset of puberty:
o Onset of puberty is due to two theories:
§ Maturation of the CNS affecting GnRH neurones (increased release).
§ Altered set-point to gonadal steroid negative feedback. - decreasing sensitivity of GnRH to gonadotrophins- leading to more gonadal secretions
o Not sure what triggers this but may be environmental.

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14
Q

Describe the changes in menarche in recent years

A

However there is evidence of a secular trend towards earlier puberty which suggests environmental factors :
improved health care
improved socio-economic factors (photoperiod? nutrition?)
§ Menarche – the first occurrence of menstruation.
o Has decreased over the last 150 years but seems to have been levelling off recently.
§ Possibly decreased due to nutritional reasons.
o Body weight at menarche has remained relatively constant at ~47kg over those years.

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15
Q

What is important to remember about adrenarche

A

§ Adrenarche – early sexual maturation stage (10 or 11) when DHEA DHEAS is made without cortisol.

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16
Q

Describe the key changes that take place during puberty

A

Females changes:
8+: growth of pubic hair and breast budding
10+: periods, growth, underarm hair and body shape change
12+: adult breast development
Male changes:
10+: growth of scrotum/testes and voice changes
11+: penis lengthening and growth of pubic hair
12+: growth spurt, change in body shape
13+: growth of facial hair
Differences: pubertal growth spurt earlier in females (11-13 years) than males (13-15 years)

Tanner stages of puberty

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17
Q

Describe the role of kisspeptin during puberty

A

Leptin may stimulate kisspeptin- which stimulates GnRH release
Leptin may also stimulate POMC and inhibit NPY/agRP release- further sitmulating GnRH release

o Kisspeptin stimulates GnRH and the GnRHR.
o Increased leptin can stimulate Kisspeptin and thus stimulate more GnRH.
§ Childhood obesity à early puberty

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18
Q

Summarise the role of the adrenal androgens during puberty

A

CRH - pituitary - ACTH- androtenedione and DHEA

Development of pubic hair, armpit hair and acne

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19
Q

Summarise the role of gonaotrophins during puberty

A

Gonads- sperm production and menarche
Male:
Development of:
Testes, penis and pubic hair

Females:
development of breast, ovaries and uterus.

Inhibin inhibits and activin stimulates the further development of pubic hair, armpit hair and acne.

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20
Q

What is the average age of menarche

A

Menarche: first period - starting from age 10, average 13

Year of menarche: has decreased from approx. 17 to age 13 - as a result of increased nutrition

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21
Q

Summarise the psychological changes that take place during puberty

A

Cognition e.g. morality • Identity • Increased self-awareness • Affect expression and regulation

More complex and philosophical thinking
Can see how others view them

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22
Q

Summarise the social changes that take place during puberty

A

• Family - parental surveillance, confiding • Peers • Increased importance • More complex & hierarchical • More sensitive to acceptance & rejection • Romantic relationships • Social role – education, occupation, etc

Changing relationship- increased risk of mental health disorders

Harder to navigate though more complex social interacitons- but may have got through with it during childhood- can no longer compensate.

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23
Q

Summarise the wider social influences during puberty

A

• School • Work • Culture (“teen” subculture; migration/culture) • Social influences eg unemployment, poverty/affluence, housing, neighbourhood effects

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24
Q

Outline the brain changes that take place during puberty

A

§ Grey matter decreases from 6yo à adolescence.
§ Linear increase in white matter until age 20
· ~12yo Frontal and parietal lobes develop peak.
· ~16yo Temporal lobes develop peak.
§ From puberty – increase in density of cortical white matter (more connections).
§ Pre-frontal cortex (executive function – i.e. planning) – increase in density of grey matter until puberty, then decrease.
· Dorso-lateral prefrontal cortex – last area to reach adult full density.
§ Synaptogenesis followed by pruning (synapse elimination) occurs.
§ Brain regions associated with more basic functions such as sensory and motor process mature first followed by association areas involved in top-down processing.

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25
Q

Describe the changes in cortical thickness during puberty

A

Increases from 5-9
Then decreases during adolescence as a result of pruning
Different regions attain peak cortical thickness at different times

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26
Q

Describe the developmental mismatch hypothesis

A

Developmental mismatch hypothesis: dopaminergic activity (sensation seeking) increases rapidly between ages 10 and 18, while the regulatory controls develop slower, leading to a period of risk taking behaviours (sex, delinquency, violence and self harm) when this dopaminergic activity is greater than the regulatory control (leading to poor risk assessment)
Dopaminergic activity decreases after 18

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27
Q

What is the harm of social media mediated by

A

Social media: harms mediated by
Cyberbullying
Reduction in sleep
Reduction in physical activity

Not total time spent necessarily

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28
Q

Summarise mental health during adolescence

A

Mental Health:
Diagnosable: 1/10 children 5-16 have diagnosable condition
Establishment: 1/2 all MH problems established by age 14, 3/4 by age 24

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29
Q

Describe Piaget’s stages of cognitive development

A

Piaget’s stages:
§ Birth à 2 Sensorimotor stage.
§ 2 à 7 Preoperational stage – symbolic thinking.
§ 7 à 11 Concrete operational stage – reason logically.
§ 11 à 15 Formal operational stage – abstract, idealistic and logical reasoning.

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30
Q

Describe Kohlberg’s theory of moral development

A

o Kohlberg’s theory of moral development:
§ Level 1 & 2 Pre-conventional – desire to avoid punishment.
§ Level 3 & 4 Conventional – to illicit validation from others.
§ Level 5 & 6 Post-conventional – internal moral code and independent of others.
· Sequence of this is fixed and people may never reach the highest levels.

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31
Q

Describe self-concept as a part of emotional development

A

o Self-concept – Harter’s 8-dimension model of self-concept:
§ Scholastic, job, athletic, physical appearance, social acceptance, close friends, romantic appeal and conduct of self – Some Jobs Are Pretty Shit, Can’t Really Complain.
· Self-concepts have clinical implications – 20-30% adolescents have low self-esteem which can lead to depression, anxiety, poor academia, social isolation, etc. However, people with good self-esteem can also be disposed to this!

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32
Q

Describe identity formation as a part of emotional development

A

o Identity formation – Erikson’s 8-life-span stages:
§ Don’t need to know the stages but one stage is in age’s 10-20 which is “Identity vs. confusion”.
o Identity formation – Marcia:
§ Identity diffusion (no crisis, no commitment) à identity foreclosure (no crisis, commitment) à moratorium (crisis, actively searching for identity) à identity achievement (crisis over).
· Only moratorium necessary for identity development.
· Identity is associated with higher – achievement, moral reasoning, social skills, et

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33
Q

Describe the potential changes in ethnic identity during puberty

A

o Ethnic identity – cultural minorities:
§ Integration – retain base culture, develop and maintain with mainstream culture as well. ++
§ Assimilation – lose base culture, develop and maintain into mainstream culture. -+
§ Separation – retain base culture, no development into mainstream culture. +-
§ Marginalisation – lose base culture, no development into mainstream culture.

34
Q

Describe the different social domains

A

o Social domains – adolescents and parents may have different views about who has the final say depending upon the social “domains” – friendships, clothes, etc. – mid-adolescence is most intense negotiations.

35
Q

Describe the changing relationships with peers and family during puberty

A

o Family:
§ Conflict with parents – most adolescents have good relationships, high confiding in mothers.
§ Family connectedness is associated with – reduced risk behaviours and increased self-esteem.
o Peer development:
§ Primary school (7-11) – goal to be accepted by peers, prefer same gender and gain loyalty.
§ 11-13 – expect genuineness, intimacy, common interests, emergence of cliques.
§ 13-16 – friendship goals, cross-gender relationships and develop larger groups.
§ 16-18 – emotional support expected and increase dyadic romantic ties.

o Influence:
§ Peers influence – interpersonal style, fashion/entertainment.
§ Parents influence – academic choice, career choice and future aspirations.

36
Q

Describe the gender differences in social development

A

o Gender differences:
§ Boys – less intimate, disclosing and friendships embedded in larger circles.
§ Girls – close and confiding relationships but are more brittle.

37
Q

Describe the role of school in social development

A

o School – 5 or more A*- C at GCSE factors:

§ Higher social class, girls > boys, ethnicity (Chinese > Indian > white) – combined effect = ~10

38
Q

What is important to remember about females

A

More likely to compare themselves to others and this is even more so in those who have mental health disorders
less likely to occur in boys (even those with mental health disorders).

39
Q

When are emotional disorders and any mental disorder likely to present

A

Adolescence

40
Q

When are behavioural disorders likely to present

A

Childhood

41
Q

Which disorders have equal prevalence throughout different age groups

A

Hyperactivity and other less common ones

42
Q

What is the greates cause of DALYs in adolescents

A

Non communicable diseases (NCD)
dominate
Global Burden of Disease

Mental disorders

43
Q

Describe the different features of anorexia

A

A. Restriction of energy intake relative to requirements leading to significantly low body weight in the context of age, sex, developmental trajectory and physical health.
• B. Intense fear of gaining weight or becoming fat, or persistent behaviour that interferes with weight gain. • C. Disturbance in experience of weight/shape, undue influence of wt/shape on self-evaluation, or persistent lack of recognition of seriousness of low body weight • D. Amenorrhoea NOT in DSM-5! • Subtype: Restricting vs. Binge-eating/Purge

Important to remove amenorrhea- doesn’t take into account boys, girls or post-menopausal women

No weight criteria - should be when it causes impairment for that patient

differ from avoidance restrictive food disorder as in anorexia- fear of gaining weight and negative affect on body image- important to understand why negative affect is on body image.

44
Q

Describe a formulation framework for anorexia

A

Individual ,familial or systemic factors which can be:
Predisposing, precipitating, perpetuating or protective

Predisposing factors: genetics (70% heritable)
Precipitating factors: weight related bullying, societal factors, depression, peers
Perpetuating factors: isolation, feeling of control, response of others
Protective factors:

Can have psychological, biological or social factors instead

45
Q

Describe LD score regression

A

Genetic correlations between anorexia nervosa and variable phenotypes
personality, psychiatric, educational ,weight and BMI related, insulin and glucose related, lipoprotein and cholesterol.

46
Q

Outline a schemata for the etiology of anorexia nervosa

A

Genetic factors and other prenatal factors (such as influence of hormones)
Both of these influence our traits and cognitive style (obsessionailty, perfectionism ,deficits in social cognition, inflexibility)
These can influence diet, potentially leading to weight loss, this can lead to starvation induced changes, leading to increased anxiety, depression and obsessionality, driving the cycle

Note puberty via brain development, hormones, stressful life events and cultural values influence this cycle

two outcomes- recovery or chronic illness as a result of starvation- induced changes

47
Q

Describe gender attitudes towards changes in body weight

A

For boys: the changes of puberty e.g. increased height, and musculature are welcomed, and are associated with increased status and athletic prowess.
a lot feel fat, few diet and a lot want to gain weight

For girls: the changes of puberty e.g. increased adiposity are may be associated with ambivalent feelings, in view of the negative attitudes to plumpness, and ambivalent feelings about onset menarche.
A lot feel fat, a lot diet and very few want to lose weight

48
Q

Describe the ethnic variation in perception of body image

A

Cultural variation: white English girls are more negative about body shape and weight than African Caribbean girls. Negative attitudes increase as weight and body mass index increase.
Asian similar to whites,
similar trend with boys

49
Q

Describe the epidemiology of anorexia nervosa in females

A

Dislikes weight, severe dieting unhealthy behaviour e.g. vomiting, laxatives etc 10%
AN + BN +1-2%

50
Q

Describe how we can predict for eating problems

A
  • Adolescent eating problems (symptoms) associated with: • Earlier pubertal maturation, & higher body fat (also extremely low BMI)
  • Concurrent psychological problem e.g. depression • Poor body image • Specific cognitive phenotypes
51
Q

Describe the neuropsychology of anorexia nervosa

A

• Association anorexia nervosa and ASD • Weak central coherence in ED’s • Global processing difficulties [review] • Poorer global processing =>Weak central coherence • Impaired set shifting

Executive function defects

When asked to draw a complex diagram- will focu on one part perfectly- inability to see bigger picture- weak central coherence.

52
Q

Summarise the evidence for treatment of anorexia nervosa

A

…..most young people who have parental/carer support with AN should be offered AN focussed family therapy (FT-AN or FBT) in conjoint, separated or multifamily format as first line treatment on an outpatient or if too sick, day patient basis, following a brief (<3 week admission) for medical stabilisation if needed

Treatment: focus on the perpetuating (maintaining) factors, as these are most likely to be modifiable

53
Q

Describe the prognosis of anorexia nervosa

A

• About 40% respond to first line interventions alone • Up to 80% recover overall within 5 years • Around 30% develop binge eating at some point during recovery • Around 20% run a more chronic course • Mortality e.g. at 20 years: 5-10% of which 1 in 5 is suicide • Duration of illness predicts recovery therefore adolescent onset better prognosis because earlier help seeking • Early treatment response is the only robust predictor of outcome but more extreme social difficulties are a factor

54
Q

Describe some other treatment options and causes of anorexia nervosa

A

Treatment
Family intervention
For abnormal eating attitudes and depression: cognitive behavioural therapy.
Small % need admission for weight restoration

Causes
Genetic predisposition, perfectionist temperament, specific subcultures, childhood abuse and adversities; perhaps higher social class.

55
Q

Describe the two concepts of depression

A

Dimension:
Continuum, increased symptoms lead to increased impairment
Category:
Disorder present or not

56
Q

What are the 3 core symptoms of depression

A

• Low mood/sadness • Loss of enjoyment (anhedonia) • Loss of energy

57
Q

Describe some other symptoms of depression

A

• Changes to: • Appetite / Weight-( / ) • Sleep- ( / ) • Concentration • Thoughts: Pessimism, Guilt • Self esteem/confidence • Libido • Psychomotor agitation/retardation • Self harm / Suicide

58
Q

Describe the key features of depression

A 
Symptoms pervasive (present all the time) • Impairing • Present for at least 2 weeks 
• Symptoms and impairment distinguish mild, moderate &amp; severe
59
Q

Describe the different types of depression

A

• Depressive episode (~ 50% recur) • Recurrent depression • Dysthymia (low mood, which may ameliorate)• Bipolar depression • Psychotic depression • Atypical depression • Seasonal affective disorder (SAD) • ?Inflammatory subtype

60
Q

Describe the problems associated with depression

A

• Increased risk of self-harm • Association with anxiety disorders; eating disorders [females]; conduct problems; substance misuse • Familial aggregation (genetic and learning)

61
Q

Describe the 1st type of pre-pubertal depression

A

• 1st: • More common presentation is with co-morbid behavioural problems, parental criminality, parental substance abuse and family discord • Course of this resembles that of children with conduct disorder • No increased risk of recurrence in adult life

Essentially, a bad-upbringing

62
Q

Describe another type of pre-pubertal depression

A

• Less common • highly familial with multigenerational loading for depression • High rates of anxiety and bipolar disorder and • Recurrences of depression in adolescence and adulthood#
§ Irritability instead of sadness (especially in boys), social withdrawal.
§ Outcome with high recurrence and impairment in later adult relationships.

63
Q

Describe how we classify the different levels of depression

A

o (1) Persistent sadness or low mood and/or;
o (2) Loss of interest or pleasure – anhedonia.
o (3) Fatigue/low-energy – anergia.
§ At least 1 of the above, most of the time for at least 2 weeks and some associated symptoms:
· (4) Disturbed sleep, (5) poor concentration, (6) low self-confidence, (7) changes in appetite and weight, (8) suicidal thoughts/acts, (9) agitation, (10) guilt or self-blame – these changes may be positive or negative (i.e. weight gain or loss).
§ Total 10 symptoms then classify level of depression - <4 (not), 4 (mild depression), 5-6 (moderate), 7> (severe).

64
Q

Summarise the symptom clusters of depression

A

§ Symptom clusters – the 10 symptoms but clustered:
o Affective – sadness, loss of enjoyment, irritability.
o Cognitive – self-blame, hopelessness, guilt.
o Biological – disturbed sleep, reduced appetite.

65
Q

Describe the developmental conisderations for depression

A

§ Developmental consideration – as you develop, these happen which may predispose to depression:
o Endocrine – especially in females and may increase risk of low mood.
o Relationships with family – get closer with family as you develop à more conflict.
o Peers – increased involvement with peers as you develop à more rejection and conflict.
o Responsibilities and hassle.

66
Q

Describe adolescent depressive disorder

A

• Irritability instead of sadness/low mood Especially in boys • Somatic complaints and social withdrawal are common • Psychotic symptoms rare before mid-adolescence

67
Q

Describe the different outcomes for adolescent depressive disorder

A

Short term • High rates of persistence and recurrence (20% in 1 yr) Lewinson et al, 1994 • Long term • Significant continuity adolescence  adulthood • Adolescent Depressive Disorder •  40-70% recurrence in adulthood •  2-7x increased risk as an adult • Impairment relationships/education in adulthood

68
Q

Outline a schemata for the developmental changes and vulnerability to depression

A

Biological changes -genetics -Puberty -Brain growth
Social changes -Peer -Family -Social world
Life events losses

All influence
Psychological/cognitive emotional changes -More advanced & efficient -More intense/fluctuant mood -Self concept, autonomy
Which influences
vulnerability to depression

69
Q

Summarise the treatment for depression

A

•Mild depression • Cognitive behavioural therapy [Individual or group] • Interpersonal psychotherapy for adolescents • Brief Psychosocial Intervention •Moderate-Severe Depression • Antidepressants e.g. SSRI’s: fluoxetine • Could be SSRI + CBT • Combined treatment  highest rate of symptomatic remission in 37% combined vs 20% fluoxetine alone

70
Q

Describe the prognosis of depression

A 
Prognosis
Major depression: Duration
In specialist CAMHS settings: 6-9 months
Primary care: 2-3 months
High risk recurrence
Prepubertal onset – better prognosis
Small number in adolescence – bipolar (mania, hypomania)
71
Q

Describe the epidemiology of depression

A

2-5% of adolescents

72
Q

Describe the different terms for conducting disorder

A

Psychiatry- conducting disorder
delinquency/offending- law
anti-social behaviour- society

73
Q

Define conducting disorder

A

Repetitive & persistent (> 6 months) pattern of dis-social, aggressive or defiant behaviour • Frequency & severity beyond age appropriate norms.
• No sharp dividing line!

Persistent failure to control behaviour appropriately within socially defined rules.

74
Q

State some common behaviours in condutcing disorder

A

Oppositional behaviour, defiance Tantrums Excessive levels of fighting or bullying, assault Running away from home Truancy Cruelty to animals Stealing Destructiveness to property Fire-setting

75
Q

Describe some different types of conducting disorder

A 
CD confined to the family context 
Unsocialized CD
Socialized CD
Oppositional CD
Depressive CD
Hyperkinetic CD
76
Q

Describe the epidemiology of conducting disorder

A

• Conduct Disorder is commonest psychiatric disorder of childhood. • National Survey of Child Mental Health (2017) • About one in twenty (4.6%) 5 to 19 year olds had a behavioural disorder, with rates higher in boys (5.8%) than girls (3.4%) • Increases with age • More common in urban than rural communities • Anti-social behaviour • Adolescent-limited • Life course persistent

77
Q

Describe the different causes of CD

A
  1. Genetic – weak
  2. Child – difficult temperament (ADHD)
    Family – poor parenting, discord, lack warmth, inconsistent discipline, coercive interaction, aggression
  3. Wider environment
    poor schools
    neighbourhoods (gang culture in cities)
78
Q

Describe the developmental considerations of CD

A

Changes in family relationships – less direct surveillance, physical closeness, joint activities
Peers – increased involvement with peers; may amplify antisocial behavior
Experimentation and risk taking – rule violation, drugs & alcohol, petty offending frequent.

79
Q

What else is CD associated with

A 
4% at ages 5-10 years; 6% at ages 10-15 years; overall 5% at ages 5-15 years.
Higher in deprived inner-city areas
Boys: girls 3:1
Age of onset may vary
Associated with
Larger family size
lower socio-economic status
80
Q

Summarise the different interventions for CD

A

Should be targeted at major modifiable risk factors and should begin at an early age
• Managing underlying hyperactivity
• Parenting programmes
• Cognitive problem-solving skills training
• Interventions at school
• Multi-systemic therapy

81
Q

Summarise the key issues with the prognosis of CD

A

• 40% of 7 and 8 year olds with CD became recidivist delinquents as teenagers. • Over 90% of recidivist juvenile delinquents had conduct disorder as children. • Predictor of • Antisocial PD in adulthood (~50%) • Alcoholism & drug dependence • Unemployment and relationship difficulties • Intergenerational transmission • HENCE IMPORTANCE OF PREVENTION!

82
Q

Describe the prognosis of CD

A

Poorer outcome with more problems in child, and family
Risk of antisocial personality disorder in males
Range of emotional and personality disorders in females

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