Plenary Discussion 1st Week

GROUP 13C:
HANIFAH PUTRI DWIRIDAL
MEGA UTAMI MULYADI
TEGUH BEDI PUTRA
MASYITAH NAQIA
VANESHA AZZURA
AULIA RAHMI SAFITRI
KARINA JULITA
FADHILA ANAS Z
M. DAVIN PUTRA R
CHYNTIA FITRI
 STEP 4: Scheme

Hormonal Anamnesis Andi,7th yo

contraception (His Mother) Boy(?)

Squatting urination

Androgen Hypospadia Workup: Gender determination

(Testosteron) Micropallus Referral Karyotyping
Undescended Testis Radiology check-up
SRY gene analyze
Leydig Cell
Multidicipline
Coordination
Testis SRY gene
Complication
Example: Infection,
psychological abnormality
 STEP 5: Learning Objectives

Definition to prognosis of male urogenital congenital

abnormalities
1. Phimosis and paraphimosis(4A)
2. Cryptochirdismus (2)
3. Hypospadia (2)
4. Testicular torsio

Definition to prognosis of female urogenital congenital

abnormalities
PHIMOSIS
Classification:
 Only after the age 16, it is considered as Phimosis in adults. It has two
types:
1. Congenital or physiological Phimosis
- As mentioned above, in all males the complete retraction of prepuce is
acquired in the age of 13 to 16 years, but some male do not acquire retraction
of prepuce after that age. It is classified as congenital.

2. Pathological Phimosis
- It is due to injury or infection. Most of the time, it is not possible to
differentiate between the two.
There are 5 grade of it, which are as follows:
 Grade 1: Full retraction of prepuce, but tightly and with small
discomfort.
 Grade 2: Half retraction. Only half of glans penis is visible after
retraction.
 Grade 3: Little less than half retraction, only meatus can be seen.
 Grade 4: Very less open, minimal distance seen between glans and
opening of prepuce.
 Grade 5: No retraction. Foreskin attached to glans.
 Epidemiology:

The prevalence of adhesions between prepuce and

glans are age dependent:
-58% after 1 year of life,
-10–35% after 3 years of life.
The prevalence of true phimosis (with scarring):
-8% in 6-year old boys
-1% with 16 years of age.
 Etiology:

Infectious
Inflammatory
Hormonal disorders
Poor hygiene
Repeated catheterization
Pathophysiology:
 Symptoms:

Unable of retraction of prepuce (The most common and important

symptom.)
Ballooning of prepuce while urination (In complete Phimosis, prepuce
opening swells and shows the appearance of the balloon while urination.)
Pain in urination
Blood in urine
Frequent urine infection and balanitis (infection of penis head or glans)
Pain or inability of sex (This is because of forceful retraction of penis)
White ring (Opening of prepuce shows some white spot, these spots are fibrosis
of the previous scar).
Obstructive voiding dysfunction
 Diagnosis:

Physical examination: foreskin is not retractability

Urine test
General blood test to exclude infection and to test for
the presence of glucose (sugar).
A swab from the foreskin area to check bacterial
culture might also be taken.
 Treatments:
Steroid cream for phimosiS
Phimosis cream is the combinations of steroid. Application of steroid cream (such
as betamethasone- dexamethasone etc) reduces inflammatory reaction and it also
relaxes prepuce opening.
Phimosis stretching
Gently stretching of the foreskin, after application of the cream, gradually relaxes
muscle.
Antibiotics
They treat infection of glans or UTI.
Phimosis Surgery
Partial or complete circumcision is the last and effective treatment for it.
 Complications:

Paraphimosis
Penile carcinoma
Recurrent balanitis
Urinary tract infection
Sexually transmitted disease
Urine retention
Undescended Testis SKDI 2
 Introduction

Cryptorchidism :
• Cryptos : Hidden
• Orchis : testicles
Synonim : Undescended testis (UDT)

Cryptorchidism :
The testicles are located in the normal desensus path, but
don’t reach normal places in the scrotum
 Epidemiology

Incident 1: 20.000 neonates

Monocydism 1: 5000  frequently on the left side
Incident Rate Cryptorchidism :
• Neonatus < 2500 g : 30,3 %
• Neonatus > 2500 g : 3.4 %
• < 12 month : 1.8 %
• > 12 month : 0.8 %
• Adult : 0.8 %
 Etiology and Risk Factor
Testicular desensus to the scrotum for the last 3 months intrauterine, most completed at
born
4 - 6%: testicular desensus is not complete at birth
20-30% premature with BB <2500 g cryptorchidism

There are 3 factors that play a role in the process of testicular descent:
Anti Mullerian hormone (AMH)
Intra-abdominal pressure
Androgen hormone factor

So, Maldensus testis happened caused by :

Abnormality gubernaculum testis
Intrisic Factor
Deficiency of Gonadotropin Hormon
 Pathogenesis & Pathophysiology

There is a normal temperature difference in the testes  Abnormal

Testicular germ cell damage :
2 years : 1/5 testicular damage
3 years : 1/3 testicular damage
N-years : Progresif and decreased
Testicular become smaller
Easily goes to :
Torsio Testis
Trauma Damage
Maligna degeneration
 Clinical Manifestation and Diagnosis
Anamnesis :
Neonatus : cannot find a testes
Adult : Infertility
Physical Examination :
Milking action
Inspection scrotum regio
Supporting Examination :
Chromosomal examination
HCG Examination  DD
Radiology : CT-Scan, MRI, X-Ray
Venography and Arteriography
Laparoschophy  Exploration
 Treatment : Surgery
If it does not go down spontaneously at the age of 6 months (according to the correction of
gestational age), surgery is performed at <12 months of age
the cryptorchidism is palpated, the surgical department will perform an orchidopexy
scrototal or inguinal action (for manipulation and fixation of the testicles in the scrotum).
cryptorchidism that is not palpated, the surgical department will perform an examination
under anesthesia for
re-evaluation of probable palpable testes. But if it remains not palpated, exploration is
carried out and if indicated can be performed abdominal orchidopexy. And need to identify
the description of the testicular blood vessels to determine the next action.
For boys with normal contralateral testes, the surgical section will perform an orchectomy if:
Testicular blood vessels and vas deferens are very short.
Dysmorphic or very hypoplatic testes.
Postpubertal age
 Treatment : Hormonal

Therapy can be give on 9 month :

• Human chorio gonadotropic hormone (HCG)
• Luteinizing-hormone-releasing-hormone (LHRH)
• Combination
 Prognosis and Complication

Infertility
Malignancy : 10 – 50 x normal
Torsio Testis
Psychological side
Iatrogenic : Orchidopexy complication
Hypospadias
 Definition

Hypospadias is an abnormality of anterior urethral

and penile development. The urethral opening is
ectopically located on the ventral aspect of the penis
proximal to the tip of the glans penis, which, in this
condition, is splayed open.
 Epidemiology

In several countries, the incidence of hypospadias may be

rising. In general, the frequency seems rather constant, at 0.26
per 1000 live births in Mexico and Scandinavia and 2.11 per
1000 live births in Hungary.

The incidence of hypospadias is higher in whites than in

blacks, and the condition is more common in those of Jewish
and Italian descent. A genetic component may be present in
certain families; the familial rate of hypospadias is about 7%.
Classification
 Sign and Symptoms
Opening of the urethra at a location other than the
tip of the penis
Downward curve of the penis (chordee)
Hooded appearance of the penis because only the
top half of the penis is covered by foreskin
Abnormal spraying during urination
 Etiology and Risk Factor
Several etiologies for hypospadias have been suggested, including genetic, endocrine, and
environmental factors.
Genetic factors
The prevalence of hypospadias in male children of fathers with hypospadias has been reported
as 8%, and 14% of brothers of children with hypospadias are also affected. The inheritance is likely
polygenic.

Endocrine factors
A decrease in available androgen or an inability to use available androgen appropriately may result
in hypospadias. In a 1997 report by Aaronson et al, 66% of boys with mild hypospadias and 40%
with severe hypospadias were found to have a defect in testicular testosterone biosynthesis.

Environmental factors
Endocrine disruption by environmental agents is gaining popularity as a possible etiology for
hypospadias and as an explanation for its increasing incidence.
 Pathophysiology

The urethral folds fuse to form a seam of epithelium, which is then

transformed into mesenchyme and subsequently canalizes by apoptosis or
programmed cell resorption. Similarly, this seam theoretically also
develops at the glanular level, and the endoderm differentiates to
ectoderm with subsequent canalization by apoptosis.
The prepuce normally forms as a ridge of skin from the corona that
grows circumferentially, fusing with the glans. Failure of fusion of the
urethral folds in hypospadias impedes this process, and a dorsal hooded
prepuce results. On rare occasions, a glanular cleft with intact prepuce
may occur, which is termed the megameatus intact prepuce (MIP) variant.
 Diagnose
Diagnose hypospadias based on a physical exam

Physical Examination
Although the appearance of hypospadias has been identified with both antenatal fetal
ultrasonography (US) and magnetic resonance imaging (MRI), the diagnosis is
generally made upon examination of the newborn infant.

Renal ultrasound is recommended to detect other anomalies in the urinary tract in

hypospadias patients. Karyotyping is recommended in patients with ambiguous
genitalia or cryptochirdism. Some tests such as electrolytes, 17-hydroxyprogesterone,
testosterone, luteinizing hormone, follicle-stimulating hormone, sex-hormone binding
globulin, and some genetic tests are considered whenever possible.
 Treatment

Several stages of surgery need to be done such as

●orthoplasty (Chordectomy) which is doing chorde
correction so that the penis can be perpendicular again
●urethroplasty, which makes a new urethra that is in
accordance with its locatio
●Glansplasty, which is the formation of penile glans
back. Glansplasty is often followed by prepucioplasty.
 Complications

The complication rate in boys with distal hypospadias

repair is less than 1 in 10. Problems happen more often
after a proximal correction.

The most common problem after surgery is a hole

("fistula") forming in another place on the penis. This is
from a new path forming from the urethra to the skin. Scars
can also form in the channel or the urethral opening
 Prognosis

With modern anesthetics, instruments, sutures,

dressing materials, and antibiotics, hypospadias repair
is considered generally successful.
Testicular Torsion
 Definition

Also referred to as torsion of the spermatic cord.

An emergency condition due to rotation of
the testis and consequent strangulation of its
blood supply.
 Epidemiology

The predisposing anomaly is present in about 12% of

males. Torsion is most common between the ages of
12 and 18, with a secondary peak in infancy. It is
uncommon in men > age 30.
It is more common in the left testis.
 Etiology

Hypermobile testis
Polyorchidopathia
Anomalous, Bifurcation and Short spermatic cord
Clapper Bell Deformity
Cold (temperatures below 15 Celcius)
 Pathogenesis

Torsion results from twisting of the spermatic cord,

which causes ischemic changes such as swelling,
degeneration, necrosis, and infarction, depending on
the degree and duration of twisting.
The degree of the torsion varies from 180 to more than
720
This contributes to hemorrhage, edema, ecchymosis,
and cellulites.
 Physical Examination

1. The Scrotal Skin is erythema, discoloration, swelling

(more than 12 hours).
2. The Position of the testicle is elevated with a horizontal.
3. The “Blue Dot Sign”
4. Acute Severe pain in Skrotum area
5. No Fever
6. Palpation: The Coil of spermatic cord
 Adjunctive Testing

MRI
USG Doppler
 Treatment

The critical time for testicular alvage has been

reported at about 6 hours.
Manual detorsion of the testis
orchiectomy
CONGENITAL ABNORMALITIES
ON WOMEN'S REPRODUCTION
 Vulva

Hymen Imperforatus
Atresia Labium minus
Hypertrophy Labium minus
Duplication of Vulva
Hypoplation of Vulva
Perineum disorder
 Hymen Imperforatus

Hymen (Hymenoralis) with no holes

Unknown before menarche (mens first time)
Menstrual blood collecting in the vagina  himen
stand out and appear bluish (hematocolpos)
Action: hymenectomy (Incision himen)
Himen
Imperforata Genitalia eksterna
Hematokolpos

Himenektomi
Insisi himen
If Hematocolpos is not resolved  utero cavum will
be filled with menstrual blood and will enlarge 
Hematometra
 Vaginal

Vaginal septum
Aplasia and Vaginal atresia
Vaginal cysts
 Vaginal septum
 The sagittal partition on the vagina
 Etiology: Disorders in the fusion or canonization of both
duct mulleri
 Rarely raises complaints  sometimes arises Dispareuni
(pain during the bun)
 Newly discovered during gynecologic examination
 Normal menstruation
 When childbirth can be ripped spontaneously
Septum Vagina
 Vagina aplasia/Vaginal agenesis

No vagina or just a shallow basin

Etiology: Duct Mulleri After fusion does not develop
and does not conduct canonization
Usually accompanied by a an rudimentary uterus
(not developed)
Action: vaginal manufacture (Neo vagina)
Agenesis vagina
Neo vagina (pembuatan vagina)
 Vaginal cysts

There are 2 kinds of cysts

1. From the remnants of the epithelial duct mulleri
2. From the remnants of the duct Gardner located in
anterolateral Vagina

Action: Removal of the cyst by taking the capsule

 UTERUS AND FALLOPIAN TUBES

Congenital abnormalities of the uterus and tuba due

to impaired growth of Mulleri duct, namely:
1. No formationThe duct of Mulleri
2. Disturbances in the canonization after fusion
 Bikornu Uterus

Bikornu Unikolis
(1 cervix, 2 horns, 1 kav
uteri, 1 tuba, 1 ovary
Bikornu Bikollis (Didelphys uterus)
2 separate sections, 2 vagina, 1 vagina with a
partition
 Uterine arcuatus

On the fundus it appears that the basin passed into

septum
 Impact on pregnancy and menstruation

25% can be pregnant and regular maternity

Menstruation: Dismenorrhea, Menorrhagia,
Metrorragia
Sex Hub: Dyspareunia
Infertility
 Ovarian

No ovarian growth occurs infrequently

When there is usually accompanied not the growth of
the tubes Also
 Congenital abnormalities of the reproductive system due to chromoson
abnormalities

Turner syndrome (45 XO)

Super Female (47 XXX)
Kleinefelter syndrome (47 XXX)
Down syndrome (trisomy 21)
Edward syndrome (trisomy 18)
Por syndrome (trisomy 13)
 Turner syndrome (45 XO)

Female, short (< 150 cm)

Primary Amenorhea
Pterigium Colli (webbed neck)
Nevus (small moles)
Aortic coarctation
Valgus Kubitus
Secondary genital does not grow
Genitalia Externna does not grow
Normal intelligence
Webbed neck
 Disorders caused by hormonal influence

Masculinization in women with female

chromosomes (Adrenogenital hyperplasia
syndrome)
Testicular feminization syndrome (male genotypes,
female phenotype)
 Adreogenital syndrome

Hipertrofi klitoris
Testicular feminization

Female traits
No radiology interna
Woman
There are testicles (in the
abdomen, or on the
inguinal canalis, in
Labium Mayus)
Good mamma growth
 Management

Must be carefully and thoroughly (chromosome

examination, hormonal, interna and external
radiology)
Determination of the status of women/men must be
carefully