adolescence and puberty Flashcards

1
Q

define adolescence *

A

the phase between childhood and adulthood

pubertal development might be the start

adulthood is legally, culturally and biologically variable

UN say adult is 18yrs

the definition is extending from 10-20, to 10-25 - this is called the new adolescence

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2
Q

why is the definition of adolescence changing *

A

the milestones that are meant to happen in adolescence ie marriage, childbirth and leaving home are happening at older ages

ie it is taking longer to master the tasks of adolescence

refers to the period of development that occurs between ages 12-18 years.

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3
Q

what are the changes that occur in adolesence *

A

cognitive and emotional changes

  • hormone driven
  • reasoning gets more abstract/phylosophical - change in cognitive capacity
  • greater knowledge/awareness of the world
  • identity of self, family, ethnicity develops
  • reflective functioning/mentalising - self awareness - see yourself through other people’s eyes

biology

  • puberty/endocrine changes
  • physical growth

family

  • challenging rules
  • discipline needs reasoning
  • less confiding and intimacy in parents
  • develop individualism and autonomy

peers

  • peer activities/confiding
  • sexual relationships
  • peer group influences values and behaviour
  • influences the development of mental health difficulties
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4
Q

describe adrenarche *

A

starts female 6-9yrs, males 7-10 ie before puberty

there is a rise in adrenal 19-carbon steroid production, dehydroepiandrosterone (DHEA) and DHEA sulfate - drives hair

purpose is uncertain but it is the precurser to puberty

it is adrenal gland driven

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5
Q

describe the hormone pathway in adrenarche *

A

CRH released from hypothalamus - acts on pit

pit produces ACTH

ACTH acts on the adrenal cortex

cause production of androsteindione and DHEA

leads to development of pubic hair, armpit hair, acne (acne is a testosterone related SE)

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6
Q

describe the endocrinology of puberty *

A

GnRH released from hypothalamus - act on pit

LH and FSH released from pit, act on gonads

gonads produce androgen and sperm in males and oestrogen and ovum production and menarche in females

androgens cause penis development, pubic hair, testes, acne

oestrogen causes development of breasts, ovaries, uterus

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7
Q

describe the growth pattern in puberty *

A

girls grow in early puberty age 12/13

boys grow late puberty age 15

therefore between ages of 12-15 girls are more developed

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8
Q

define menache *

A

first period

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9
Q

what are the main female changes in puberty *

A

breast budding

growth of pubic hair

growth spurt

menache

underarm hair

change in body shape

adult breast size

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10
Q

level of puberty at age 13 for girls *

A

can be prepubertal or fully adult - both are normal

delayed puberty doesnt mean that you have anormal growth

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11
Q

changes that happen in puberty in boys *

A

growth of scrotum and testes

change in voice

lengthening of the penis

growth of pubic hair

growth spurt

change in body shape

growth of facial and underarm hair

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12
Q

describe how menarch has changed over time *

A

age of puberty has reduced

because of nutrition

if overweight there is an earlier puberty - increased leptin = increased stimulatioon of kisspeptin neurons = increased GnRH

however, population studies have suggested body weight at menarche has remained constant

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13
Q

psychological changes that occur in puberty *

A

cognition eg morality/ethics - higehr levels of cognitive ability - piaget’s psychological changes

identity - gender and religion

increased self awareness

affect expression and regulation - learn to recognise and manage emotions

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14
Q

social changes that occur in puberty *

A

family - parents need to give you respect and autonomy, you are less confiding however need good connections and surveillance - the quality of the time becomes more important than the quantity

peers - increased importance, more complex relationships, hierarchial, more sensitive to acceptence and rejection (trigger for mental health), romantic relationships

social role - education, occupation

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15
Q

what becomes apparent at puberty socially *

A

deficits in interpersonal skills

before you are protected by family and understand concrete things

now world becomes more complex so might have subtle communication difficulties that make it difficult for you to communicate with peers and form relationships

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16
Q

wider social influences in adolesence *

A

school

work

culture - teen subculture, migration/culture

social influences eg unemployment, poverty/affluence, housing, neighbourhood effects

social media

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17
Q

describe the effect of social media on mental health *

A

it isnt the time that you spend on it

it is whether it is beiung used as cyber bullying, stopping you sleep or exercise

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18
Q

describe the development of the brain in adolescence *

A

there is cortical thickening and then thinning in adolesence

there is a cross over from grey to white matter - this is pruning

the neurons that are used dominate, those that are not are pruned

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19
Q

effect of developmental change in brain on behaviour *

A

there is a mismatch

there is a period where the dopaminergic/opiodinergic activity ie sensation seeking is ahead of the regulatory/cognitive control to think rationally

therefore it isnt that more risks are taken in adolesence its just that there is a miscalculation of risks

these behaviours might continue into adolesence

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20
Q

incidence of mental health disorders in children

A

1/10 children aged 5-10 - most are neurodevelopmental disorders rather than emotional

1/2 of mental health disorders are established by 14

3/4 by 24

some are episodic and relapsing, rather than chronic and persistant

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21
Q

describe the association between comparing self on social media and psychiatric disorder *

A

of people who compare themselves on social media there is a higher proportion of people with psychiatric disorder than not

this is even more common in girls

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22
Q

when do emotional disorders emerge *

A

in teenage years

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23
Q

how does mental health disease relate to the burden of disease globally *

A

it is the dominant disease in terms of burden

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24
Q

define the features of anorexia *

A

restriction of energy intake relatuve to the requirements leading to significantly low body weight for the person in the context of age, sex and developmental trajectory and physical health

psychopathy - intense fear of ganing weight or becoming fat, or persistant behaviour that interfers with weight gain

disturbance in experience of weight/shape - undue influence of weight or shape on self-evaluation or persistant lack of recognition of seriousness of low weight

weight loss is self induced

endocrine disturbance - amenorrhoea, or delayed growth and puberty - not necessary for diagnosis

dont have to be able to articulate why acting in certain way - drs can infer by the fact they are avoiding calorie dense food

subtypes - restricting v binge eating/purge - they have different prognosises

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25
Q

describe the formulation framework to determine the cause of anorexia *

A

look at predisposing (background factors that increase the risk), precipitating (the trigger), perpetuating (what keeps it going), protective features (tell you about the prognosis) and determine if they are bioological, family or systemic factors (or can be individual/psychological/social)

eg genetic risk is predisposing family

precipitating is systemic precipitating

there is not 1 cause and it is different for each person

26
Q

example of predisposing factors *

A

bullying, genetics

27
Q

describe the genetic contribution to anorexia nervosa *

A

there are psychological risks

cognitive style risks

metabolic risks

ie there is a psychosomatic risk profile

ie the hertability is multideterminant - about 50-70%

we can modify some of the factors but mainly have to work with the non-heritable ones these are the non-shared factors (ie things that only effect the individual, not other people in their system)

28
Q

what are precipiatitating factors *

A

interpersonal things

29
Q

what are perpetuating factors *

A

people’s responses to you determine the outcome so need to involve family in treatment

perpetuating factors are the things that can be modified in treatment

30
Q

summarise the aetiology of anorexia nervosa (

A

they go through prenatal, childhood, adolesence, adulthood

genetic factors, traits and cognitive style (obsessionality, perfectionism, deficits in social cognition, inflexibility), hormones, puberty (brain development, hormones, stressful life events, cultural values)

being female

traits lead to dieting and weight loss

perhaps higher social class

leads to starvation induced changes eg aberrent reward response to starvation syndrome

which increases anxiety, depression and obsessionality

31
Q

describe the fact that anorexia nervosa is on a scale of being normal *

A

>50% girls feel fat

a lot of girls diet

only a small amount of people want to put on weight

boys ahve the same feeling but are less inclined to diet - perhaps because less influenced by social media

boys have a stringer wish to gain muscle - this is body dysmorphic disorder

the feeling of being fat is present across cultures and countries

32
Q

what are the proportions of girls with unhealthy eating behaviour *

A

30-50% dislike weight etc

10% of these have severe dieting and unhealthy behaviour eg laxatives

1-2% of them have anorexia/bulieia - it is hard to knwo what the threshold of normal is

20% of girls have obesity

33
Q

what can be used to predict eating problems *

A

it is associatyed with:

  • Earlier pubertal maturation, & higher body fat - the thin and the overweight are those at most risk
  • Concurrent psychological problem e.g. depression - hating the world is a risk factor but need to determine why that has become about food (usually it is because of poor body image)
  • Poor body image
  • Specific cognitive phenotypes
34
Q

describe the neurophysiology of anorexia nervosa - executive functioning deficits *

A

thinks that borderline autistic traits increase risk of AN because world narrows to be focused on food etc

however - we all become narrow minded and focussed when starved so difficult to know if narrow minded because starved or because you are predisposed to it

people have weak central coherence ie global processing difficulties - they dont see the big picture and have coherent fixed thinking

35
Q

describe why there is an incidence in obesity and eating disorders *

A

the things that drive obesity also drive eating disorders - ie dieting and body image/satisfaction

36
Q

treatment for eating disorders *

A

when pts have parental/carer support they should have an anorexia focused family therapy - either in conjoint, separated, or multifamily format as 1st line as an out patient

or if too sick as a day patient following a <3wk admission for medical stabalisation if needed

For abnormal eating attitudes and depression: cognitive behavioural therapy.

37
Q

prognosis for anorexia

A

About 40% respond to first line interventions alone

Up to 80% recover overall within 5 years when you add something in

Around 30% develop binge eating at some point during recovery

Around 20% run a more chronic course then can doe - higehr death rate than T1DM/asthma

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

38
Q

what are the 2 ways to classify depression *

A

dimension - an increase of symptoms means an increase in impairment

category - whether the disorder is present or not

39
Q

symptoms of depression *

A

affective - low mood/saddness, loss of enjoyment (anhedonia), loss of energy, irritability

leads to changed in:

  • biological - appetite/weight, sleep
  • concentration
  • cognitive - pessimism/guilt/self blame
  • self esteem/confidence
  • libido
  • psychomotor agitation/retardation
  • self harm/suicide

have to have a collection of the symptoms in order to have a disorder

40
Q

what is necessary to ‘have’ depression *

A

need a collection of the symptoms

they need to be pervasive - feel the same whereever the situation, even if masked

impairing fuinction

present for at least 2 wks

the symptoms and impairment determine whether you have mild/moderate/severe

41
Q

what are the differnet types of depression *

A

Depressive episode - 20% people have an episode, 50% of these people have a recurring episode

Recurrent depression - between episodes there are periods of remission

Dysthymia - consistently low mood but gets better/worse over time

Bipolar depression - be down then up

Psychotic depression - hallucinations

Atypical depression

Seasonal affective disorder (SAD)

?Inflammatory subtype

42
Q

problems associated with depression *

A

increased risk of self harm

association with anxiety disorders, eating disorders, conduct problems, systems missuse

familial aggregation (genetic and learning) - the influence of environment

43
Q

what are the 2 types of pre-pubertal depression *

A

1

  • more common
  • present with co-morbid behavioural problems, parental criminality, parental substance misuse and family discord
  • course resembles that of people with conduct disorder
  • there is no increased risk of recurrence in adult life - more likely to go into conduct disorder pattern

2

  • less common
  • highly familial - multigenerational loading for depression
  • high rates of anxiety and bipolar disorder
  • social withdrawal
  • recur in adolesence and adulthood
44
Q

describe adolescent depressive disorder *

A

irritability instead of sadness/low mood

especially in boys

somatic complaints and social withdrawal are common - feel bad feeling in stomach, gut extension of forebrain so have feelings there

psychotic symptoms are rare before mid-adolescence

45
Q

outcome of adolescent depressive disorder *

A

short term - high rates of persistence and recurrance - 20% in 1yr

long term - 50% continuity into adulthood, 2-7x increased risk as an adult, impairment of relationships/education in adulthood

46
Q

causes of depression *

A

biological changes - genetics, puberty, brain growth, endocrine change in female risk low mood

social changes - peer, family, social world

life events - losses

these all feed into psychological/cognitive emotional changes - more advanced and efficient, more intense/fluctuant mood, self concept/autonomy

cause a vulnerability to depression

life events eg exams, adversities

47
Q

treatment of mild depression *

A

cognitive behavioural therapy

interpersonal psychotherapy for adolescents

brief psychosocial intervention - supportive therapy

family intervention for associated family problems

48
Q

treatment of moderate-severe depression *

A

antidepressants eg SSRIs - fluoxetine

could be antidepressant and cognitive behavioural therapy

combined has the highest rate of symptomatic remission

49
Q

what is conduct disorder *

A

repetitive and persistant (>6months) pattern of antisocial behaviours at frequency and severity beyond age appropriate

behaviours:

  • 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
50
Q

what are the types of conduct disorders *

A

CD confined to family setting

unsocialised CD

socialised CD

oppositional CD

depressive CD

hyperkinetic CD

(depends on whether you do it on your own/in peer group - unsocialised is worse prognosis )

51
Q

what is the epidemiology of CD

A

about 5% of 5-19yr odlds had CD, higher in boys, increases with age, more common in urban than rural communities

either adolescent limited or life course persistant

52
Q

aetiology of CD*

A

child factors - eg ADHD, educational drop out due to unrecognised learning disabilities, impulsivity, difficut temprement

family factors - inadequate parenting, discord, lack warmth, inconsistent discipline, coercive interaction, aggression

environmental factors eg inner city/access to specific peer gps - gang culture

genetic - weak

53
Q

intervention for CD (

A

targeted at major modifyable risk factors - should begin early

managing underlying hyperactivity

parenting programs

cognitive problem solving skills training

interventions at school - restorative justice intervention

multisystemic therapy

54
Q

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
55
Q

hormones involved in growth *

A

androgens and somatotrophin

56
Q

how does puberty start *

A

either:

  • Maturation of the CNS affecting GnRH neurones (increased pulsatile release)
  • Altered set point to gonadal steroid negative feedback
57
Q

how does puberty affect anorexia in girls *

A

in puberty there is increased adiposity causing an increase in negative attitudes in white people, less so in afrocaribbean people

58
Q

prognosis of depressive disorder *

A

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)

59
Q

developmental considerations for 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.

60
Q

epidemiology of conduct disorder

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