The average age range of attaining physical changes of puberty in boys is:
C. The average age at which physical changes of puberty occur is different for boys and girls. Tanner staging is often used to assess physical changes in puberty and stage 2 genital changes are used to define onset of puberty. It varies between 11 and 13 in girls, and 13 and 17 in boys. It must be noted that the criteria that more accurately reflect gonadal activity are breast development in girls and genital growth in boys. As these are difficult to ascertain, reliable measurement is not possible using observations of physical maturity; puberty as assessed by hormonal measurements of the hypothalamic pituitary gonadal axis is well established before physical signs appear.
Reference:
The proportion of children with childhood autism that show improvement by the age of 6 years is:
E. By the age of 6 years, 10–20% of individuals with autism begin to improve. Eventually 15% of individuals achieve satisfactory self-sufficiency while another 20% manage with minimal periodic support. The remainder of at least 60%individuals does not achieve sufficient self sufficiency for an independent life. This outcome is variable according to degree of communicative language developed and IQ.
In families with one autistic child, the risk of a further autistic child is about:
B. In families with one autistic child the risk of a further autistic child is around 3 – 5%. This sibling risk rate for autism denotes a tenfold increase over general population rates. Epidemiological studies of same sex autistic twins have identified around 60% monozygotic concordance while 0% for dizygotic twins. This difference becomes further pronounced when a broader autistic phenotype of related cognitive or social abnormalities are considered (92% of MZ pairs vs. 10% of DZ pairs). The risk to a monozygotic co-twin is estimated to be over 200 times the general population rate.
The estimated heritability of attention deficit hyperactivity disorder (ADHD) is around:
E. The heritability of ADHD is estimated to be around 70%. Twin studies performed in several countries have shown that the average genetic contribution is 70–80% while non genetic variance contributes to 20–30%. It is also observed that 6% of adoptive parents of ADHD probands have ADHD compared to 18% of the biological parents of ADHD probands and 3% of the biological parents of the control probands. Siblings of children with hyperkinetic disorder have a 2–3 times greater risk of the disorder than siblings of normal controls.
References:
All of the following factors predict poor outcome in conduct disorders except:
A. Childhood conduct disorder can continue as adult antisocial personality disorder. A wide range of other psychiatric disorders including substance abuse, major depression, psychosis and various adverse outcomes such as suicide, delinquency, educational difficulties and unemployment have been associated with conduct disorder. Evidence on prognosis of conduct disorder suggests dose-response relationship: The higher the number and variety of disruptive behaviours, the worse the adult outcomes. But most adolescents with conduct disorder do not develop antisocial personality in adulthood. Those who do not develop adverse outcomes as adults are most likely to have a late onset, adolescent-limited disorder rather than a life-course persistent problem with early onset. Other poor prognostic factors include severity, comorbid hyperactivity, pervasive behavioural disruption across varied settings and continuous exposure to risk factors.
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