Fechamento tutoria SP1 Md2

1) Hebe, a deusa grega da juventude, serviu de inspiração para o nome da

especialidade, que existe desde 1974 — seu primeiro curso surgiu em
São Paulo, na Faculdade de Medicina da USP, difundindo-se no Rio e
em outras partes do país. Para receber o título de hebiatra, o médico
precisa cursar dois anos de especialização em pediatria e mais dois de
especialização em medicina do adolescente.

Segundo a Organização Mundial da Saúde (OMS), a adolescência vai dos

10 aos 20 anos. As especificidades do grupo decorrem, de um lado, do
processo de crescimento e desenvolvimento, que implica necessidades de
monitoramento e suporte a aspectos morfofuncionais, mas, sobretudo, aos
aspectos socioculturais relacionados a esse processo. Por essa razão, as
definições de adolescência e juventude, normalmente utilizadas no campo
da saúde, levam em consideração: os marcos pubertários e de crescimento
e desenvolvimento, as experiências de vida em contexto, envolvidas no
adolescer, como também os limites cronológicos associados às normas
civis e jurídicas socialmente estabelecidas (Saito, Silva, Leal, 2008;
Coates, Beznos, Françoso, 2003).

No Brasil, os principais critérios delimitadores nas práticas em saúde são

os da Organização Mundial da Saúde (OMS) e os do Estatuto da Criança e
do Adolescente (ECA) (Brasil, 2010). Segundo a OMS, a adolescência
corresponde à segunda década da vida, de dez a 19 anos, e a juventude vai
dos 15 aos 24 anos (OMS, 1975). Para o ECA, a adolescência é a fase
situada entre 12 e 18 anos de idade, com algumas exceções, em que o
estatuto se refere a pessoas de até 21 anos (Brasil, 1990).

A hebiatria, campo do conhecimento médico que estuda a saúde e a

doença na adolescência, define essa fase como o momento de transição
da infância à adultícia. Aponta a puberdade, dimensão biológica,
corporal desse processo de maturação, como um marcador físico do
mesmo, que não se restringe a ela. A puberdade manifesta-se mais
claramente pelos primeiros sinais da maturação sexual; isto é, pelo
surgimento dos primeiros caracteres sexuais secundários: na menina, o
aparecimento do broto mamário; e, no menino, o aumento do volume
testicular (Setian, Colli, Marcondes, 1979)
2) A puberdade é o fenômeno biológico que se refere às mudanças
fisiológicas e morfológicas resultantes da reativação dos mecanismos
neuro-hormonais do eixo hipotalâmico-hipofisário-gonadal. As
principais manifestações da puberdade são o estirão puberal e as
mudanças na composição corporal, além do desenvolvimento gonadal,
dos órgãos de reprodução, das características sexuais secundárias e dos
sistemas e órgãos internos. Ocorre grande variabilidade no tempo de
início, na duração e na progressão do desenvolvimento puberal.

A monitorização do desenvolvimento puberal é feita pela classificação

de Tanner, que estudou e sistematizou a seqüência dos eventos puberais
em ambos os sexos, em cinco etapas, considerando, quanto ao sexo
feminino, o desenvolvimento mamário e a distribuição e a quantidade de
pêlos; e no masculino, o aspecto dos órgãos genitais e também a
quantidade e a distribuição dos pêlos pubianos.

A representação gráfica do estagiamento de Tanner para mamas no sexo

feminino encontra-se na Figura 1.

• M1 – mama infantil. • M2 (8-13 anos) – fase de broto mamário, com

elevação da mama e aréola como pequeno montículo. • M3 (10-14 anos)
– maior aumento da mama, sem separação dos contornos. • M4 (11-15
anos) – projeção da aréola e das papilas para formar montículo
secundário por cima da mama. • M5 (13-18 anos) – fase adulta, com
saliência somente nas papilas. Na Figura 2 podemos observar as
diversas fases de desenvolvimento puberal, levando-se em consideração
os pêlos pubianos em ambos os sexos e a genitália no sexo masculino.
Sexo feminino • P1 – fase de pré-adolescência (não há pelugem). • P2
(9-14 anos) – presença de pêlos longos, macios e ligeiramente
pigmentados ao longo dos grandes lábios. • P3 (10-14,5 anos) – pêlos
mais escuros e ásperos sobre o púbis. Figura 1 – Mamas Figura 2 –
Pêlos pubianos nos sexos feminino e masculino • P4 (11-15 anos) –
pelugem do tipo adulto, mas a área coberta é consideravelmente menor
que a do adulto. • P5 (12-16,5 anos) – pelugem do tipo adulto, cobrindo
todo o púbis e a virilha. Sexo masculino • P1 – fase de pré-adolescência
(não há pelugem). • P2 (11-15,5 anos) – presença de pêlos longos,
macios e ligeiramente pigmentados na base do pênis. • P3 (11,5-16
anos) – pêlos mais escuros e ásperos sobre o púbis. • P4 (12-16, 5 anos)
– pelugem do tipo adulto, mas a área coberta é consideravelmente
 menor que a do adulto. • P5 (15-17 anos) – pelugem do tipo adulto,
estendendo-se até a face interna das coxas. Genitália (sexo masculino) •
G1 (9,5-13,5 anos) – pré-adolescência (infantil). • G2 (10-13,5 anos) –
crescimento da bolsa escrotal e dos testículos, sem aumento do pênis.

8) e 9)
The male reproductive system consists of the testes, the internal
genitalia (accessory glands and ducts), and the external genitalia.
The external genitalia consist of the penis and the scrotum, a saclike
structure that contains the testes.
The urethra serves as a common passageway for sperm and urine,
although not simultaneously. It runs through the ventral aspect of the
shaft of the penis (Fig. 26-8 *) and is surrounded by a spongy column
of tissue known as the corpus spongiosum [corpus, body; plural
corpora].
The corpus spongiosum and two columns of tissue called the corpora
cavernosa constitute the erectile tissue of the penis. The tip of the penis
is enlarged into a region called the glans that at birth is covered by a
layer of skin called theforeskin, or prepuce.
The male accessory glands and ducts include the prostate gland, the
seminal vesicles, and the bulbourethral (Cowper s) glands. The
bulbourethral glands and seminal vesicles empty their secretions into
the urethra through ducts. The individual glands of the prostate open
directly into the urethral lumen.

The scrotum is an external sac into which the testes migrate during fetal
development. This location outside the abdominal cavity is necessary
because normal sperm development requires a temperature that is 2° 3° F
lower than core body temperature.

The failure of one or both testes to descend is known as cryptorchidism

[crypto, hidden * orchis, testicle] and occurs in 1 3% of newborn males. If
left alone, about 80% of cryptorchid testes spontaneously descend later.
Those that remain in the abdomen through puberty become sterile and are
unable to produce sperm. Although cryptorchid testes lose their sperm-
producing potential, they can produce androgens, indicating that hormone
production is not as temperature sensitive as sperm production.

The testes have a tough outer brous capsule that encloses masses of coiled
seminiferous tubules clustered into 250 300 compartments (Fig. 26-
9b).Between tubules is interstitial tissue consisting primarily of blood
vessels and the testosteroneproducing Leydig cells (Fig. 26-9c).

The seminiferous tubules constitute nearly 80% of the testicular mass in an

adult. The seminiferous tubules leave the testis and join the epididymis
[epi-, upon + didymos, twin], a single duct that forms a tightly coiled cord
on the surface of the testicular capsule (ig. 26-9b).

The epididymis becomes the vas deferens [vas, vessel + deferre, to carry
away from], also known as the ductus deferens. This duct passes into the
abdomen, where it eventually empties into the urethra, the passageway
from the urinary bladder to the external environment (see Fig. 26-8).
Seminiferous Tubules

The seminiferous tubules are the site of sperm production and contain two
types of cells: spermatogonia in various stages of becoming sperm and
Sertoli cells (Fig. 26-9c, d).

The developing spermatocytes stack in columns from the outer edge of the
tubule to the lumen. Between each column is a single Sertoli cell that
extends from the outer edge of the tubule to the lumen. Surrounding the
outside of the tubule is a basal lamina (Fig. 26-9d) that acts as a barrier,
preventing certain large molecules in the interstitial fluid from entering the
tubule but allowing testosterone to enter easily.

Adjacent Sertoli cells in a tubule are linked to each other by tight junctions
that form an additional barrier between the lumen of the tubule and the
interstitial uid outside the tubule. These tight junctions are sometimes
called the bloodtestis barrier because functionally they behave much like
the impermeable capillaries of the blood-brain barrier, restricting
movement of molecules between two compartments.

Sertoli Cells

The function of Sertoli cells is to regulate sperm development. Another

name for Sertoli cells is sustentacular cells because they provide
sustenance, or nourishment, for the developing spermatogonia. Sertoli cells
manufacture and secrete proteins that range from the hormones inhibin and
activin to growth factors, enzymes, and androgen-binding protein (ABP).
ABP is secreted into the seminiferous tubule lumen, where it binds to
testosterone (Fig. 26-11 *). Protein binding makes testosterone less
lipophilic so that it cannot diffuse out of the tubule lumen.

Leydig Cells

Leydig cells, located in the interstitial tissue between seminiferous tubules

(Fig. 26-9c, d), secrete testosterone. They are rst active in the fetus, when
testosterone is needed to direct development of male characteristics. After
birth, the cells become inactive until puberty, when they resume
testosterone production. The Leydig cells also convert some testosterone to
estradiol.
Spermatogenesis Requires Gonadotropins and Testosterone

The hormonal control of spermatogenesis follows the general pattern

described previously: hypothalamic GnRH promotes release of LH and
FSH from the anterior pituitary (Fig. 26-11). FSH and LH in turn stimulate
the testes.

The gonadotropins were named originally for their effect on the female
ovary, but the same names have been retained in the male. GnRH release is
pulsatile, peaking every 1.5 hours, and LH release follows the same pattern.
FSH levels are not as obviously related to GnRH secretion because FSH
secretion is also influenced by inhibin and activin.

The target of FSH is Sertoli cells because (unlike oocytes) male germ cells
do not have FSH receptors. FSH stimulates Sertoli synthesis of paracrine
molecules needed for spermatogonia mitosis and spermatogenesis. In
addition, FSH stimulates production of androgen-binding protein and
inhibin.

The primary target of LH is the Leydig cells, which produce testosterone.

In turn, testosterone feeds back to inhibit LH release.

Testosterone is essential for spermatogenesis, but its actions also appear to

be mediated by Sertoli cells. Spermatocytes have no androgen receptors
and cannot respond directly to testosterone, but they do have receptors for
androgen-binding protein. Sertoli cells, which produce androgen-binding
protein, have androgen receptors.

Spermatogenesis is a very dif cult process to study in vivo or in vitro, and

the available animal models may not accurately reflect the situation in the
human testis.

6) Sperm Production

Spermatogonia, the germ cells that undergo meiotic division to become

sperm, are found clustered near the basal ends of the Sertoli cells, just
inside the basal lamina of the seminiferous tubules (Fig. 26-9c, d).

In this basal compartment, they undergo mitotic divisions that produce

additional germ cells. Some of the spermatogonia remain near the outer
edge of the tubule to produce future spermatogonia. Other spermatogonia
enter meiosis and become primary spermatocytes.

As spermatocytes differentiate into sperm, they move inward toward the

tubule lumen, continuously surrounded by Sertoli cells. By the time
spermatocytes reach the luminal ends of Sertoli cells, they have divided
twice and become spermatids.

Spermatids remain embedded in the apical membrane of Sertoli cells while

they complete the transformation into sperm, losing most of their
cytoplasm and developing a agellated tail (Fig. 26-10 *). The chromatin of
the nucleus condenses into a dense structure, while a lysosome-like vesicle
called an acrosome attens out to form a cap over the tip of the nucleus. The
acrosome contains enzymes essential for fertilization. Mitochondria to
produce energy for sperm movement concentrate in the midpiece of the
sperm body, along with microtubules that extend into the tail [ p. 65]. The
result is a small, motile gamete that bears little resemblance to the parent
spermatid.
 3) Androgens Influence Secondary Sex Characteristics

Androgens have a number of effects on the body in addition to

gametogenesis. These effects are divided into primary and secondary sex
characteristics.

Primary sex characteristics are the internal sexual organs and external
genitalia that distinguish males from females. As you have already learned,
androgens are responsible for the differentiation of male genitalia during
embryonic development and for their growth during puberty.

The secondary sex characteristics are other traits that distinguish males
from females. The male body shape is sometimes described as an inverted
triangle, with broad shoulders and narrow waist and hips. The female body
is usually more pear shaped, with broad hips and narrow shoulders.
Androgens are responsible for such typically male traits as beard and body
hair growth, muscular development, thickening of the vocal chords with
subsequent lowering of the voice, and behavioral effects, such as the sex
drive, also called libido [libido, desire, lust].

Androgens are anabolic hormones that promote protein synthesis, which

gives them their street name of anabolic steroids. The illicit use of these
drugs by athletes has been widespread despite possible adverse side effects
such as liver tumors, infertility, and excessive aggression ( roid rage).

One of the more interesting side effects is the apparent addictiveness of

anabolic steroids. Withdrawal from the drugs may be associated with
behavioral changes that include depression, psychosis, or aggression. These
psychiatric disturbances suggest that human brain function can be
modulated by sex steroids, just as the brain function of other animals can.
Fortunately, many side effects of anabolic steroids are reversible once their
use is discontinued