Everything turns on where the failure sits and which way the gonadotropins move. If the testis itself fails, testosterone drops and the pituitary shouts louder, driving FSH and LH up; that is the $hypergonadotrophic$ pattern. If the pituitary or hypothalamus is at fault, the gonadotropins stay low; that is the hypogonadotrophic pattern.
Part (a) asks for the misfit among hypergonadotrophic causes. Mumps and other viral orchitis scar the testis, Klinefelter's 47,XXY leaves small fibrosed testes, and Noonan syndrome is often tied to primary testicular dysfunction; all three raise gonadotropins. Kallmann's is built differently, a defect in GnRH neuron migration paired with loss of smell, so its gonadotropins are LOW. That makes Kallmann's the exception.
Part (b) asks for the commonest primary testicular cause. Klinefelter's syndrome tops that list and is the leading congenital cause of male hypogonadism overall. The printed sheet mislabels part (b) as hypogonadotrophic, but Klinefelter's is unambiguously a primary, high gonadotropin disorder, so the medically sound reading keeps Klinefelter's as the commonest hypergonadotrophic cause.
For this combined row the lead is part (a), whose exception is Kallmann's.
\[\boxed{\text{(a) Kallmann's syndrome; (b) Klinefelter's syndrome}}\]