AULIA RISMA L - 012116339
“Mengapa saya belum hamil”
Step 1
Infertiitas : ketidakmampuan pasangan suami istri untuk memiiki keturunan waupun sudah melakukan senggama sebanyak 2-3 kali/minggu dalam waktu satu tahun
Primer : belum pernah hamil
Sekunder : sudah pernah meahirkan tapi tidak hamil lagi
Step 2 1. Apa pengaruh pekerjaan terhadap keluhan pasien ? 2. Apa hubungan uretritis GO dengan infertilitas ? 3. Apa hubungan infertilitas dengan BB pada suami dan istri ? 4. Apa hubunan suami perokok berat dan alkohol dengan skenario ? 5. Apa hubungan suami berendam air panas dengan infertilitas ? 6. Apa hubungan pemeriksaan penunjan istri igG positiv untuk citoplasma rubella , sitomegaovirus? 7. Apa hubungan pemberian kntrasepsi awal dengan skenario ? 8. Apa hubungan umur dengan infertilitas ? 9. Apa penyebab infertiitas ? 10.Faktor resiko terjadi nya infertilitas ? 11.Jenis-jenis infertilitas ? 12.Pemeriksaan apa saja untuk menunjukaninfertiitas 13.Bagaimana cara mendiagnosis infertilitas ? 14.Bagaimana penanganan infertilitas?
Step 3 1. Apa pengaruh pekerjaan terhadap keluhan pasien ?
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Wanita Tingkat stresskeuar kortisolpengaruhi fase vulasipemendekan fase luteal
Pria sering dudukpengaruh suhu harus lebih rendah 3-4 derajat skrorumberpengaruh untuk jumlah sperma
Pria aktv berlebihan susah untuk membuahi ovum
Suhu rendahtestis mengkerut
Suhu panasmengendor
2. Apa hubungan uretritis GO dengan infertilitas ?
Kompikasisal sperma inferksimempengaruhi dari viabilitas sperma
Infeksi pengaruh DNA kualitas sperma rusak
3. Apa hubungan infertilitas dengan BB pada suami dan istri ?
Suami 30obesitas 1
Istri 29 preobesitas
PriaGemuklemak banyakkumpul pada pubispenis kecilhub pasifkesulitas penetrasi
Lemak banyakmengubah h.testoteron menjadi estrogen menekan produksi FSH dan LH sel sertolispermatogenesis
FSHmerangsang sel legdi
LH testoteron memberi umpan balik negatif ke hipofisis anterior
Wanitasteroidgenesisdi ubah
4. Apa hubunan suami perokok berat dan alkohol dengan skenario ?
Gaskarbonmonoksidaradikal bebasstres oksidatifmenganggu spermakerusakan memban dan viabilitas
Gasradikal bebasregulasi fungsi sperma
Peningkatan 8hidroksidioksivanoksineada kerusakan anti oksida DNA kromatin berubah
Dampak mengurangi produksi lambat dan aliran darah ke testis terhambat
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Wanitamengubah siklus mestruasimetabolisme di hati berlebihhepar rusakpengaruh testoteroninfertilitas
Produksi ATP di mitokondria terganggusperma beraglutinasi
Pengaruh SSPpengaruh hipofisis dan hipotalamus GNRH terganggutidak peka kerja tidak maksimal produksi terganggu
Alkoholfungsi liver tergangguestrogen lebih tinggikelainan sperma
5. Apa hubungan suami berendam air panas dengan infertilitas ?
Pembentuk spema berendam di air panas dapat melemaskan ototseringskrotummengurangi pembentukan sperma
Proses hipoksia sel testisenzim yang merusak sel germinal terlalu lama berendam air panas DNA rusak
6. Apa hubungan pemeriksaan penunjan istri igG positiv untuk toksoplasma , rubella , sitomegalovirus?
IgG positif kronik
Jika menginfeksitrjd sumbatanovum yang di hasil kan ovarium tidak bisa keluar
Getah servik asamsperma masuk mati
IgM infeksi primer
7. Apa hubungan pemberian kontrasepsi awal dengan skenario ?
I thn menundabelum tahu sampe kapan minum pil
8. Apa hubungan umur dengan infertilitas ?
Wanita->25-30 thn paling bagus
Priasampai 40 thn
Wanitaumur 30 thn frekuensi senggama menurun
Pria umur 40 thn frekuensi senggama menurun
9. Apa penyebab infertiitas ?
Priaf. 40%
Wanitagangguan ovulasi10%
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
adesi pelvis 20
problem lendir servik 5
faktor lain dan imunologi 5
tidak diketahui sebabnya
wanitaovarium gagaltidak terjjadi ovulasi
tuba falopi berkelok2 tersumatinfeksi
pria o keadaan diluar testis
kelainan endokrin: hipofisis dan hipotalamus
kelainan kelanjar adrenal
kelainan farikokelberkelok
funikulus spermatikus : absen duktus deferen tidak
posttestikular tersamung
kelainan prostat dan vesikulasseminularis
kalainan penis dan uretra
faktor tertikular : kriptokismus, torsi,tumor
kegagalan menghasilkan sperma yang berkualitascacat bawaan
gangguan pengeluaran spermaggn seksual ejakulasi dini
faktor gaya hidupmakanan, obbesitas , polusi udara
ggn terkaid kanker dan pengobatan
analisis cairan seminaljumlah spermatozoa kurang
jumlah sperma Abnormal belebihi 40
cairan seminal yang di ejakulasi kurang 2 ml cairan kimia tidak memuaskan faktor ejakulasi
f. Fisikhipospadia.epispadia
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
f.psikologistres
alkohol kronis
faktor2 penyebab infertilitas 10.Faktor resiko terjadi nya infertilitas ?
Wanita semakin tua umur 40semakin lama konsepsi
Laki frek koitus berkurang
Frek koitus korelasi positif antara frek koitus dgn angka kehamilan
Masa koitus ovulas hari ke 10-15 maksial ovulasi
Lubrican
Merokok atau alkohol berlebihan buruk kuaitas sperma
11.Jenis-jenis infertilitas ?
Primer pasutri tidak pernah konsepsi meskipun senggama teratur lebih 12 bulan tnp perlindungan
Sekunder pernah mengalami konsepsi sebelumnya tp kemudian tidak mampu meskipun senggama teratur lebih 12 bln tnp perlindungan
Kehamilan sia2 istri mampu hamil tp tidak sampai genap bulan
Infertilitas tak terjelaskanbelum di temukan , tidak pernah konsepsi
Subfertilkesulitan konsepsi bersama karena fertilitas kedua kurang
Infertilitas umum tidak mampu hamil . mengandung genap bulan , mengndung ayi hidup atau suami tidak mampu menghamili istri
12.Pemeriksaan apa saja untuk menunjukan infertiitas ?
Pria analisis sperma , saluran sperma ,normal 100-120 juta/cc
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Wanita pemantauan ovulasipenelitian riwayat siklus haid, lendir servik,pemantauan siklus basal , biopsi endometrium, pemeriksaan hormon
13.Bagaimana cara mendiagnosis infertilitas ?
Anamnesishub brp kali seminggu , rokok, alkohol , siklus haid
Pemeriksaan fisikpanggul
penunjang
14.Bagaimana penanganan infertilitas?
Spema obat-obat
Saluran sperma operatif
Edukasimerokok dan alkohol pada pria
Bayi tabung
Definisi infertilitas Hubungan pemakaian pil kb dengan infertilitas Kaitan konsumsi rokok Kebiasaan berendam diri diair panas Faktor apa saja penyebab infertilitas pada wanita Mekanisme terjadinya infertilitas pada laki Penatalaksaaan infertilatas laki-laki Penatalaksaaan infertilatas wanita Laki-laki 34 tahun , perokok, alkohol,
Perempuan 29 tahun
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Step 7 1. Apa pengaruh pekerjaan terhadap keluhan pasien?
Male Arguably of more concern are lifestyle and occupational factors that cause men to spend a long time in a sedentary position, something that has become common for many men working in Western countries today (figure 2). When seated, air does not circulate so easily around the scrotum and therefore there is less-efficient cooling, an effect likely to be exacerbated if wearing tight underpants or trousers. (http://rstb.royalsocietypublishing.org/content/365/1546/1697.full.p df) Female Stress causes an increased secretion of hypothalamic corticotropinreleasing factor, increased pituitary adrenocorticotropic hormone
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
release, and augmented secretion of adrenal cortex hormones, including cortisol. Therefore, it can be assumed that stress has a direct effect on cortisol level production and therefore, a negative effect on fertility. High circulating stress hormones can interfere with the timing of ovulation and shorten the luteal phase. Diminished progesterone availability in the luteal phase post-conception lessens the likelihood of a successful implantation; a 12-day luteal phaseand ≥8 mm endometrial thickness have been put forward as minimums for fertility. Accordingly, the circulation of elevated levels of stress hormones during the period between pre-conception and early pregnancy
may
prevent
implantation
and
early
pregnancy
maintenance by luteal phase defect mechanisms. (http://www.mjpsychiatry.org/index.php/mjp/article/viewFile/101/93 ) Stress dapat menyebabkan anovulasi dan amenore. Ketegangan emosional
mungkin
disertai
dengan
disfungsi
seksual
seperti
vaginismus dan dispareunia. Impotensi seringkali berkaitan dengan stress. Terdapat laporan kasus azoospermia yang disebabkan oleh kecemasan berat, yg reversible saat stress dihilangkan. (Seri Skema diagnosis dan penatalaksanaan infertlitas) 2. Apa hubungan uretritis GO dengan infertilitas? Genitourinary (GU) infections are a potential cause of male infertility. Gallegos et al. found that GU infections increase sperm DNA fragmentation and decrease sperm concentration, morphology, and motility. Appropriate antibiotic treatment of GU infections has been shown to significantly reduce sperm DNA fragmentation and improve sperm concentration and motility. https://www.clevelandclinic.org/reproductiveresearchcenter/docs/agr adoc446.pdf “Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Pada laki-laki, gonorrhea dapat menyebabkan penyumbatan vas deferens, Chlamydia dapat menyebabkan uretritis dan mycoplasma dapat mengganggu spermatogenesis. (Seri skema diagnosis dan penatalaksanaan infertlitas) 3. Apa hubungan infertilitas dengan BB pada suami dan istri? An
important
lifestyle-dependent
factor
that
adversely
affects
spermatogenesis is obesity. A BMI of more than 25 is associated with an average 25 per cent reduction in sperm count and sperm motility. A variety of explanations have been put forward to explain this association. The strongest evidence is that the alterations in sperm production are secondary to altered hormone changes. Obesity in men is associated with reduced blood testosterone levels, this reduction being proportional to the degree of obesity (e.g. Tchernofet al.1995; Gouldet al.2007; Nielsen et al.2007). In addition, there may be an increase in circulating oestradiol levels, leading to an altered testosterone : oestradiol ratio (Hammoud et al. 2006, 2008). As such patients often show reduced blood levels of LH (and FSH), when an increase might be expected in the face of reduced testosterone levels, one
interpretation
testosterone
levels
is
that
and
there
thus
is
decreased
reduced
intratesticular
androgen
drive
to
spermatogenesis. The best evidence supporting this interpretation is that suppression of oestradiol levels in obese men using aromatase inhibitors normalizes the testosterone: oestradiol ratio and improves semen quality (Raman & Schlegel 2002), and there are similar results for oligozoospermic dogs (Kawakamiet al. 2004). However, there may also
be
intratesticular
effects
that
are
unrelated
to
altered
gonadotrophin levels because the reduction in inhibin B levels in obese men is disproportionately larger than the change in FSH levels, suggesting there may be direct effects of the increased obesity on “Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Sertoli function (Jensen et al. 2004a,b; Winterset al.2006; Hammoudet al. 2008). Alternatively, it could indicate reduced Sertoli cell number in obese (young) men (Winterset al.2006). The latter is a far more serious possibility as reduced Sertoli cell number would permanently lower sperm counts as discussed earlier; it is unclear how, or when, obesity would lead to a reduction in Sertoli cell number. Another explanation for reduced spermatogenesis in obese men could be deposition of fat around the scrotal blood vessels, leading to impaired blood cooling and elevated testicular temperature Olfat 1981); the more sedentary life of obese men would probably exacerbate any temperature increase. (http://rstb.royalsocietypublishing.org/content/365/1546/1697.full.p df) Endocrine The endocrine abnormalities associated with obesity in women are well known with an increase in androgen metabolism andelevated oestrogen
levels.
demonstrate
a
similarly, relative
obese
men
have
hyperoestrogenic
been
shown
to
hypogonadotrophic
hypogonadism, with BMI being negatively correlated with testo-sterone and inhibin concentrations and positively correlated with oestrogen levels. Inhibin, which is secreted from the sertoli cells, has a direct effect on the pituitary gland in suppressing fol-licular stimulating hormone production. Inhibin B may be impor-tant as it is known to influence spermatogenesis and severely obese men have been shown to have reduced inhibin B levels. The reason why obesity causes hypoandrogenism is thought to be multifactorial. In obesity, it is known that the circulating levels of oestrogens increase due to increased aromatisation of testicular and adrenal androgens in adipose tissue. Indeed when the aromatase inhibitor letrozole was administered to obese men, testosterone levels increased and serum oestradiol levels decreased. “Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
These high oestrogen levels cause inappro-priate suppression of the hypothalamic-pituitary-gonadal
axis,
resulting
in
decreased
testosterone production. It is also possible that the elevated oestrogen levels have a direct adverse influence on spermatogenesis although the nature of this is as yet undetermined. However, whether the modest decrease in testosterone levels is responsible for suppression of spermatogenesis remains to be proven. In a recent observational study, despite demonstrating relative hypogonadotropic hypoandrogenism in obese men, semen analysis parameters were unaffected, while others have shown obesity to be associated with a decrease in testosterone and total sperm count. These opposing results, suggest that any effect of reduced testoster-one on male infertility may be modest and that further studies are required to give definitive answers. Conversely it has been suggested that rather than obesity causing impaired testicular function, defective spermatogenesis causes obesity, with some supporting evidence, such as body fat increasing in men receiving therapy to reduce testosterone during treatment for prostatic cancer. Insulin resistance is known to be associated with obesity and has been negatively correlated with testosterone levels. Interestingly in a metaanalysis of 80 articles, men with type 2 diabetes have been shown to have a lower level of testoster-one than controls. Furthermore, the spermatozoa of men with type 2 diabetes have a significantly higher level of DNA fragmentation. Another mechanism for these endocrine changes relates to sleep apnea, which is more common in obese persons. It appears to decrease the nocturnal rise of testosterone, resulting in lower morning testosterone levels, which can be reversed by weight loss.
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
4. Apa hubunan suami perokok berat dan alkohol dengan skenario?
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
Rokok Impact of cigarette smoking on reproduction in men: Men who smoke cigarettes have a lower sperm count and motility and increased abnormalities in sperm shape and function. The effect of smoking on male fertility, however, is more difficult to discern because it is difficult to create studies to address that question. Although the effects of cigarette smoking on male fertility remain inconclusive, the harmful effect of passive smoke on the fertility of female partners and the evidence that smoking adversely affects sperm quality suggest that smoking in men should be regarded as an infertility risk factor. (https://www.asrm.org/uploadedFiles/ASRM_Content/Resources/Patient_Res ources/Fact_Sheets_and_Info_Booklets/smoking.pdf)
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
(http://www.sart.org/uploadedFiles/ASRM_Content/News_and_Publications/ Practice_Guidelines/Educational_Bulletins/Smoking_and_infertility(1).pdf)
Alkohol Numerous studies have indicated that alcohol abuse in men can cause impaired testosterone production and shrinkage of the testes (i.e., testicular atrophy) (Adler 1992). Those changes can result in impotence, infertility, and reduced male secondary sexual characteristics (e.g.,
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339 reduced facial and chest hair, breast enlargement, and a shift in fat deposition from the abdomen to the hip area). This atrophy likely is caused by several factors, including (1) alcohol’s damaging effects on the testes; (2) alcohol’s effects on LH and FSH (see the section “Alcohol’s Effects on the Anterior Pituitary Gland,”pp.199–200), which, among other factors, stimulate testicular growth; and (3) various confounding factors, such as mal-nutrition, concomitant treatment with various medications, and abuse of drugs other than alcohol by the subjects. Tes-ticular atrophy results primarily from the loss of sperm cells and decreased diameter of the seminiferous tubules. Alcohol’s Effects on Leydig Cells and Testosterone Metabolism Alcohol’s
adverse
effects
on
Leydig
cell
function
and
testosterone
production. The investigators attributed the decline in testosterone to a decrease in the production rate and an increase in the breakdown and removal of testosterone from the blood (i.e., an increased metabolic clearance rate). Another mechanism through which alcohol may lower testosterone levels is the conversion of testosterone or one of its precursors into estrogens through a process called aromatization. For example, testosterone can be metabolized to an estrogen called estradiol.
Similarly,
the
immediate
precursor
of
testosterone—
androstenedione—can be converted into a less potent estrogen called estrone. This conversion process may be enhanced in men who regularly consume alcohol. Several studies found that some people with alcoholic liver disease have increased levels of estrogens in the blood (Van Thiel et al. 1974, 1978; Gordon et al. 1978). This increase does not appear to be caused by decreased estrogen breakdown and therefore must result from increased estrogen production (Gordon et al. 1978). Investigators
have
suggested
that
alcohol’s
breakdown
product,
acetaldehyde, may be a contributing factor, because in some studies
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339 acetaldehyde was more potent than alcohol in suppressing testosterone release (e.g.,Badr et al. 1977; Cobb et al. 1978). Possibly, however, acetaldehyde does not itself suppress testosterone production. Instead, the enzyme that mediates the breakdown of alcohol to acetaldehyde uses certain molecules (i.e., cofactors) that are also required by enzymes involved in testosterone production, thereby preventing testosterone generation (Ellingboe and Varanelli 1979; Gordon et al. 1980). Other studies have noted an increase in β-endorphin levels in the testicular fluid after acute alcohol exposure (Adams and Cicero 1991). As described previously, testicular β-endorphin inhibits testosterone production and/or release. Researchers recently confirmed the role of β-endorphin through a study in which rats were treated with a substance that inhibits β-endorphin activity (i.e., nal-trexone) (Emanuele et al. 1998). For example, the adrenal hormones cortisol (in humans) and corticosterone (in rats) can suppress the reproductive system by inhibiting the ability of the Leydig cells to produce and release testosterone. Studies in humans and animals found that alcohol exposure increases adrenal hormone levels, thereby interfering with reproductive functions (Rivier and Vale 1988). Moderate alcohol consumption (i.e., 40 to 80 grams, or approximately 3.5 to 7 standard drinks, per day) was associated with a slight alteration insperm maturation. Finally, a history of heavy alcohol consumption (more than 80 grams, or more than 7 drinks, per day) led to arrested sperm development in 20 percent of the cases. Studies in alcoholics who had not yet developed severe liver damage (i.e., in whom liver damage itself had not affected testicular function) found that 40 percent of the men studied had reduced sperm counts, 45 percent showed abnormal sperm shapes, and50 percent exhibited altered sperm motility (Villalta et al. 1997). The mechanisms underlying alcohol’s effects on the Sertoli cells have not yet been fully elucidated. It appears, however, that alcohol may damage some of
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339 the proteins required for sperm cell production that the Sertoli cells provide (Zhu et al. 1997). Effects on LH Production, Secretion, and Activity Conceivably, alcohol could disrupt the functioning of the GnRH receptor or its interaction with GnRH, thereby leading to diminished LH release. To date, however, scientists have found no evidence indicating that the interaction of GnRH with its receptor is impaired. Accordingly, alcohol probably interferes with one or more events that happen within the cell after GnRH has attached to its receptor. Researchers have identified one such reaction. For GnRH to stimulate the production and release of LH effectively, an enzyme called protein kinase C must move from within the LH-producing cell to the cell’s surface. Alcohol has been shown to prevent this movement of protein kinase C (Steiner et al. 1997). The chain of events from the binding of GnRH to the pituitary cell to the release of LH, however, is highly complex. Consequently, alcohol probably also interferes with other steps in this process. The identification of those steps will lead to a more complete understanding of how alcohol disrupts pituitary function. (http://pubs.niaaa.nih.gov/publications/arh22-3/195.pdf)
Penyalahgunaan alkohol dan marijuana yg berat dapat menyebabkan hipogonadisme dan spermatogenesis abnormal. Alkohol dan rokok dalam jumlah sedang tampaknya tidak memiliki efek bermakna pada kualitas semen. (Seri Skema Diagnosis dan Penatalaksanaan Infertilitas) 5. Apa hubungan suami berendam air panas dengan infertilitas? Active production of sperm requires a temperature about 3–4°C lower than normal body temperature. This fact is supported by the decreased sperm count seen in pathologies such as varicocele and cryptorchidism, as well as in cases of prolonged sauna exposure and in paralyzed patients restricted to wheelchairs. The effect of chronic occupational exposure to high
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AULIA RISMA L - 012116339 temperatures has been examined, in addition to in the welding profession, in the ceramics industry 41). Impairment of spermatogenesis has been found in a high prevalence among professional drivers, as well 42, 43). Velez de la Calle et al. 44) investigated infertilityisk factors in a French military population and found heat exposure as an independent risk factor for male infertility (OR 4.5, 95%CI 1.9–10.6), using a multivariate analysis.
(http://www.jniosh.go.jp/en/indu_hel/pdf/IH41_09.pdf)
Testicular descent into the scrotum normally occurs by birth in boys and failure of testicular descent, especially when this extends into puberty and adult-hood, results in absence of spermatogenesis. The testes descend into the scrotum in order that their temperature can be kept 3 – 4 C below core body
temperature,
as
maintenance
at
normal
body
temperature
is
incompatible with spermatogenesis (Mieusset & Bujan 1995b; Setchell 1998). As well as testis position, the two other key elements in ensuring cooling of the testis are the presence of a vascular-rich corrugated scrotal surface via which heat loss can occur and the presence of an arterio-venous plexus (the pampiniform plexus) in the spermatic cord and which functions as a heat exchanger to cool incoming blood to the testis by heat exchange with the cooler venous blood that is exiting the testis (Maddockset al. 1993; Pineret al. 2002). Normal functioning of this plexus is important for maintaining testicular coolness, and it is potentially susceptible to disruption by chemicals or by vascular-active drugs (Pineret al. 2002) or by disorders such as varicocele in which the veins in the plexus are varicosed (Turner 2001). However, even if the pampiniform plexus is functioning normally, it cannot cool the incoming arterial blood to the testis unless the blood leaving the testis is already itself cool, and this requires heat loss via the scrotal surface and its transmission to the underlying testes. There-fore, anything that impedes scrotal heat loss will affect testicular temperature and in turn any elevation of testicular temperature will have a harmful effect on spermatogenesis. In general, the more prolonged is the elevation in testicular temperature, then the greater will be the detrimental effect on spermatogenesis (Mieusset & Bujan 1995b; Setchell 1998).
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AULIA RISMA L - 012116339 Based on experimental studies in laboratory animals, a 30 min soak in a moderately hot bath (40 – 428C) impairs spermatogenesis (Setchell 1998) and, more importantly, it can induce germ cell apoptosis, DNA damage to the sperm and impair embryo development and fertility when ‘affected’ males are mated with normal females. These have shown that heat exposure causes hypoxia and oxidative stress responses in the germ cells, manifest as increased expression of hypoxia inducible factor 1a, haem oxygenase 1, glutathione peroxidase 1 and glutathione-S-transferase-a, which push the germ cells towards apoptosis (Paulet al. 2009). Perhaps of more concern is if mild oxidative DNA damage is induced such that the germ cells continue their development into sperm, as this is associated with increased time for such sperm to initiate a pregnancy in humans (Loftet al. 2003). (http://rstb.royalsocietypublishing.org/content/365/1546/1697.full.pdf)
6. Apa hubungan pemeriksaan penunjan istri igG positiv untuk toksoplasma , rubella , sitomegalovirus? Toxoplasma Poor obstetric outcomes, sterility and toxoplasmosis There is as yet no direct evidence showing the association between toxoplasmosis and sterility in women. Nevertheless, some studies have demonstrated that T. gondii infection could cause reproductive failure in mice, which was due to an acquired hypogonadotropic hypogonadism secondary to hypothalamic dysfunction, exhibiting histopathological changes with estrus cycling cessation, impaired folliculogenesis and few corpora lutea. It seems that T. gondii infection in pregnant women may cause
poor
obstetric
outcomes
such
as
spontaneous
abortion,
hydatidiform mole, still-born, teras and sterility. Women who had a poor obstetric outcome history had a seroprevalence of 14.2% to 33.9% which was much higher than that of the normal pregnancy in China. A survey of T. gondii infection in 68 cases of oviducal sterility revealed a prevalence of 44.1%, which was significantly different from that in “Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
normal pregnant women (3.3%), indicating that Toxoplasmainfection could result in oviducal sterility. T. gondii infection is also found to be related with the male sterility. Recent zoopery studies revealed that the reproductive parameters including sperm motility and sperm concentration were significantly decreased in T. gondiiinfected rats, and a marked increase in sperm abnormalities was also found in these infected male rats. Similar results were also observed in male mice experimentally infected with T. gondii. Zhou (2002) found thatToxoplasma infection in infertile human couples was higher than that in fertile couples, possibly related to the antisperm antibodies which were higher inToxoplasma-infected couples. A recent investigation of T. gondii infection in 100 men with sterility revealed that 16% of them were IgM-positive and 13% were CAg-positive, significantly higher than in healthy men. The seroprevalence of Toxoplasma infection in male sterility cases were 19.8% in Luoyang, Henan province, to 22.8% in Yan'an, Shaanxi province, significantly higher than in the healthy men. Based on a number of relevant studies and investigations in China, it is concluded that T. gondii infection may result in male sterility. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174123/) Toxoplasma pada pria Transmission of T. gondiioccurs via oral rout, congenital transmission, organ transplantation and rarely through blood transfusions (3). In different studies T. gondiide-tected in semen and reproductive organs of experimentally infected male rat (27), rabbit (28, 29), dog (30), goat (31, 32), sheep (33-37), cattle (38) and pig (39). There are some evidence propose that T. gondiican transmit with semen to female animals (28, 30, 36). In this regard, data obtained by Arantes et al. has clearly shown that T. gon-diiis transmitted through semen to female dog (30). In their study, T. gondiidetected in testicle, epididymis and seminal samples of experimentally infected male dogs. Moreover, the infected seminal
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
samples were injected to Toxoplasma-negative female dogs with artificial insemi-nation. They observed all of the female dogs were infect-ed. In two of the female dogs fetal reabsorption occurred at the beginning of gestation, likewise numerous Toxo-plasmic cerebral cysts were isolated from four puppies of the dogs (30). In rabbit, presence of T. Gondii DNA in semen and blood of experimentally infected male has been observed at 7 to 88 days post infection (28). The infection in some Toxo-plasma-negative female rabbits resulted from artificial insemination of infected semen has been reported by Liu et al. (29). A recent study conducted by de Moraes et al. showed that
in
sheep
artificial
insemination
of
semen
experimentally
contaminated with T. gondiitachyzoites was capable to infect sheep that suggested the possibility of venereal transmission of T. gondiiin sheep (36, 37). Fur-thermore, persistent anestrus, hydrometra, mucometra and follicular cysts along with histopathological lesions in placentas were observed in female sheep that infected with contaminated semen (36, 37). A remarkable study conducted by Dass et al. revealed that T. gondiicould transmit sexually in rats (27). In this study, T. gondiicysts were observed in epididymis and semen of infected male rats eight weeks postinfection. The cysts also observed in vaginal lavage of female rats 12 hours after mating with infected male rats resulting infection in female rats. In addition, Parasite cysts were detected in some pups of mated females. These observa-tions confirm sexually transmission of T. gondiiin rats. Moreover, comparison of mating behavior in infected and non-infected rats showed T. gondiienhanced sexual attractiveness of infected animals with manipulation of mating behavior; that means uninfected females pre-ferred infected males. So, T. gondiigained greater oppor-tunities for venereal transmission.
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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Hormonal manipulations of T.gondiimay lead to male reproductive impairment. Impairment of different hor-mones was reported during T. gondiiinfection (40-49). This impairment may cause insufficient male reproduc-tivity. Testosterone is one of the most important hor-mones that play a critical role in male fertility. Recently, Kanˇková et al. reported that the level of testosterone was decreased in T. gondiiinfected male and female mice than uninfected control animals (40). 7. Apa hubungan pemberian kontrasepsi awal dengan skenario? Wanita yg berhenti dari kontrasepsi oral memiliki interval untuk kelahiran yg lebih panjang dibandingkan dengan wanita yg menggunakan metode lain; perbedaan ini menghilang 30 sampai 42 bulan setelah menghentikan pil. Walaupun beberapa alat kontrasepsi dalam rahim berhubungan dengan penyakit peradangan pelvis, tetapi tidak terdapat efek langsung terhadap penundaan kesuburan. Tidak terdapat bukti bahwa spermisida atau cara barrier mengganggu fertilitas. (Seri Skema Diagnosis dan Penatalaksanaan Infertilitas) 8. Apa hubungan umur dengan infertilitas ?
(http://sogc.org/publications/age-and-fertility/)
As women age, fertility declines due to normal, age-related changes that occur in the ovaries. Unlike men, who continue to produce sperm “Knowing is not enough; we must apply. Willing is not enough; we must do.”
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throughout their lives, a woman is born with all the egg-containing follicles in her ovaries that she will ever have. At birth there are about one million follicles. By puberty that number will have dropped to about 300,000. Of the follicles remaining at puberty, only about 300 will be ovulated during the reproductive years. The majority of follicles are not used up by ovulation, but through an ongoing gradual process of loss called atresia. Atresia is a degenerative process that occurs regardless of whether you are pregnant, have normal menstrual cycles, use birth control, or are undergoing infertility treatment. Smokers appear to experience menopause about 1 year earlier than non-smokers.
FERTILITY IN THE AGING FEMALE A woman’s best reproductive years are in her 20s. Fertility gradually declines in the 30s, particularly after age 35. Each month that she tries, a healthy, fertile 30-year-old woman has a 20% chance of getting pregnant. That means that for every 100 fertile 30-year-old women trying to get pregnant in 1 cycle, 20 will be successful and the other 80 will have to try again. By age 40, a woman’s chance is less than 5% per cycle, so fewer than 5 out of every 100 women are expected to be successful each month. Women do not remain fertile until menopause. The average age for menopause is 51, but most women become unable to have a successful pregnancy sometime in their mid-40s. These percentages are true for natural conception as well as conception using fertility treatment including in vitro fertilization (IVF). Although stories in the news media may lead women and their partners to believe that they will be to able use fertility treatments such as IVF to get pregnant, a woman’s age affects the success rates of infertility treatments. The age-related loss of
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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female fertility happens because both the quality and the quantity of eggs gradually decline. FERTILITY IN THE AGING MALE Unlike the early fertility decline seen in women, a man’s decrease in sperm characteristics occurs much later. Sperm quality deteriorates somewhat as men get older, but it generally does not become a problem before a man is in his 60s. Though not as abrupt or noticeable as the changes in women, changes in fertility and sexual functioning do occur in men as they grow older. Despite these changes, there is no maximum age at which a man cannot father a child, as evidenced by men in their 60s and 70s conceiving with younger partners. As men age, their testes tend to get smaller and softer, and sperm morphology (shape) and motility (movement) tend to decline. In addition, there is a slightly higher risk of gene defects in their sperm. Aging men may develop medical illnesses that adversely affect their sexual and reproductive function. Not all men experience significant changes in reproductive or sexual functioning as they age, especially men who maintain good health over the years. If a man does have problems with libido or erections, he should seek treatment through his primary care provider and/or urologist. Decreased libido may be related to low levels of testosterone. EGG QUALITY Women become less likely to become pregnant and more likely to have miscarriages because egg quality decreases as the number of remaining eggs dwindle in number. These changes are most noted as she reaches her mid-to-late 30s. Therefore, a woman’s age is the most accurate test of egg quality. An important change in egg quality is the frequency of genetic
abnormalities
called
aneuploidy
(too
many
or
too
few
chromosomes in the egg). At fertilization, a normal egg should have 23 chromosomes, so that when it is fertilized by a sperm also having 23 chromosomes, the resulting embryo will have the normal total of 46 chromosomes. As a woman gets older, more and more of her eggs have “Knowing is not enough; we must apply. Willing is not enough; we must do.”
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either too few or too many chromosomes. That means that if fertilization occurs, the embryo also will have too many or too few chromosomes. Most people are familiar with Down syndrome, a condition that results when the embryo has an extra chromosome 21. Most embryos with too many or too few chromosomes do not result in pregnancy at all or result in miscarriage. This helps explain the lower chance of pregnancy and higher chance of miscarriage in older women. EGG QUANTITY The decreasing quantity of egg-containing follicles in the ovaries is called “loss of ovarian reserve.” Women begin to lose ovarian reserve before they become infertile and before they stop having regular periods. Since women are born with all of the follicles they will ever have, the pool of waiting follicles is gradually used up. As ovarian reserve declines, the follicles become less and less sensitive to FSH stimulation, so that they require more stimulation for an egg to mature and ovulate. At first, periods may come closer together resulting in short cycles, 21 to 25 days apart. Eventually, the follicles become unable to respond well enough to consistently ovulate, resulting in long, irregular cycles. Diminished ovarian reserve is usually age-related and occurs due to the natural loss of eggs and decrease in the average quality of the eggs that remain. However, young women may have reduced ovarian reserve due to smoking, family history of premature menopause, and prior ovarian surgery. Young women may have diminished ovarian reserve even if they have no known risk factors. (https://www.asrm.org/uploadedFiles/ASRM_Content/Resources/Patient _Resources/Fact_Sheets_and_Info_Booklets/agefertility.pdf) Konsepsi lebih besar kemungkinannya untuk terjadi jika suami berusia kurang dari 25 tahun dibandingkan jika suami berusia lebih dari 25 tahun, dengan penurunan jelas keberhasilan konsepsi jika suami >35 tahun. Tetapi konsepsi dapat juga terjadi pada usia lanjut saat laki-laki memiliki fungsi erektil dan kualitas semen yg minimal. “Knowing is not enough; we must apply. Willing is not enough; we must do.”
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(Seri Skema diagnosis dan penatalaksanaan Infertilitas) 9. Apa penyebab infertiitas?
Faktor penyebab infertilitas pada suami: Faktor kelainan alat kelamin: -
Hipospadia (muara saluran kemih terletak di permukaan bawah)
-
Ejakulasi retrograd (ejakulasi dimana air mani masuk dalam kandung kemih)
-
Terdapat varikokel
-
Buah zakar mengecil
-
Buah zakar yg tidak turun
Faktor Fungsional -
Kemampuan ereksi berkurang
-
Kelainan pada pembentukan sperma
-
Gangguan pada sperma dan spermatozoa
Faktor penyebab infertilitas pada istri: Anatomis: “Knowing is not enough; we must apply. Willing is not enough; we must do.”
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-
Liang senggama 5%
-
Mulut rahim (serviks) 5 %
-
Rahim sendiri 5%
-
Tuba fallopii 50-65%
-
Indung telur 10-15%
-
Faktor lapisan dalam abdomen (peritoneum) 5%
Fungsional -
Gangguan sistem hormonal wanita dan dapat disertai dengan kelainan bawaan
-
Gangguan pada pelepasan telur
-
Gangguan pada korpus luteum
-
Gangguan implantasi hasil konsepsi
10. Faktor resiko terjadi nya infertilitas? Sebagian besar pasangan dengan infertilitas sekunder menemukan penyebab masalah kemandulan sekunder tersebut, dari kombinasi berbagai faktor meliputi : 1. Usia Faktor usia sangat berpengaruh pada kesuburan seorang wanita. Selama wanita tersebut masih dalam masa reproduksi yang berarti mengalami haid yang teratur, kemungkinan masih bisa hamil. Akan tetapi seiring dengan bertambahnya usia maka kemampuan indung telur untuk menghasilkan sel telur akan mengalami penurunan. Penelitian menunjukkan bahwa potensi wanita untuk hamil akan menurun setelah usia 25 tahun dan menurun drastis setelah usia diatas 38 tahun. Berdasarkan penelitian yang dilakukan oleh National Center for Health Statistics menunjukkan bahwa wanita subur berusia dibawah 25 tahun memiliki kemungkinan hamil 96% dalam setahun, usia 25 – 34 tahun menurun menjadi 86% dan 78% pada usia 35 – 44 tahun.
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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Pada pria dengan bertambahnya usia juga menyebabkan penurunan kesuburan.
Meskipun
pria
terus
menerus
memproduksi
sperma
sepanjang hidupnya, akan tetapi morfologi sperma mereka mulai menurun. Penelitian mengungkapkan hanya sepertiga pria yang berusia diatas 40 tahun mampu menghamili isterinya dalam waktu 6 bulan dibanding pria yang berusia dibawah 25 tahun. Selain itu usia yang semakin tua juga mempengaruhi kualitas sperma ( Kasdu, 2001:63 ). 2. Masalah reproduksi Masalah pada system reproduksi dapat berkembang setelah kehamilan awal bahkan, kehamilan sebelumnya kadang-kadang menyebabkan masalah
reproduksi
yang
benar-benar mengarah
pada
infertilitas
sekunder, misalnya perempuan yang melahirkan dengan operasi caesar, dapat menyebabkan jaringan parut yang mengarah pada penyumbatan tuba. Masalah lain yang juga berperan dalam reproduksi yaitu ovulasi tidak teratur, gangguan pada kelenjar pituitary dan penyumbatan saluran sperma. 3.Faktor gaya hidup Perubahan pada faktor gaya hidup juga dapat berdampak pada kemampuan setiap pasangan untuk dapat menghamili atau hamil lagi. Wanita dengan berat badan yang berlebihan sering mengalami gangguan ovulasi, karena kelebihan berat badan dapat mempengaruhi estrogen dalam tubuh dan mengurangi kemampuan untuk hamil. Pria yang berolah raga secara berlebihan juga dapat meningkatkan suhu tubuh mereka,yang mempengaruhi perkembangan sperma dan penggunaan celana dalam yang ketat juga mempengaruhi motilitas sperma ( Kasdu, 2001:66 ).
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
AULIA RISMA L - 012116339
(Seri Skema Diagnosis dan Penatalaksanaan Infertilitas) 11. Jenis-jenis infertilitas? Jenis infertilitas ada dua yaitu
infertilitas primer dan infertilitas
sekunder.
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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Infertilitas primer adalah kalau istri belum pernah hamil walaupun bersanggama tanpa usaha kontrasepsi dan dihadapkan pada kepada kemungkinan kehamilan selama dua belas bulan. Infertilitas sekunder adalah kalau isrti pernah hamil, namun kemudian tidak terjadi kehamilan lagi walaupun bersanggama tanpa usaha kontrasepsi dan dihadapkan kepada kemungkinan kehamilan selama dua belas bulan.
(Seri Skema Diagnosis dan Penatalaksanaan Infertilitas) 12. Pemeriksaan apa saja untuk menunjukan infertiitas? Pemeriksaan Dalam
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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Diharapkan memberikan gambaran tentang alat kelamin wanita secara umum, yaitu liang senggama, kelainan mulut rahim, kelainan pada rahim, kelainan pada saluran telur, pemeriksaan sonde. Pemeriksaan terhadap ovulasi Dilakukan untuk membuktikan ovulasi. Tindakan ini dilakukan dengan anggapan bahwa pada pemeriksaan dalam tidak didapatkan kelainan. -
Pemeriksaan suhu basal Dengan terjadinya pelepasan telur, suhu basal badan menjadi bifasik sehingga saat perubahan itulah harus dimanfaatkan untuk melakukan hubungan seks dengan kemungkinan hamil yg besar.
-
Uji lendir serviks dan sitologi vagina Lendir serviks menjelang ovulasi menjadi jernih, daya membenang bertambah.
-
Biopsi endometrium
Pemeriksaan terhadap saluran telur -
Pemeriksaan partubasi memasukkan gas CO2 ke dalam rahim, mulut rahim, dan tuba.
-
Pemeriksaan hidrotubasi memasukkan cairan kombinasi antibiotik, preparat kortison, dan akua steril dalam jumlah sekitar 10-20cc melalui mulut rahim, rahim, dan selanjutnya tuba fallopii gangguan ditandai dengan keluarnya kembali cairan tersebut melalui liang senggama.
-
Pemeriksaan histerosalpingografi memasukkan bahan kontras ke mulut rahim, sampai ke tuba, selanjutnya difoto rontgen.
Pemeriksaan khsus -
Pemeriksaan histeroskopi
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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Memasukkan
alat
optik
ke
dalam
rahim
untuk
mendapatkan
keterangan tentang mulut saluran telur dalam rahim, lapisan dalam rahim, dan keterangan lain yg diperlukan -
Pemeriksaan laparoskopi Memasukkan alat optikdalam ruang abdomen untuk mendapatkan keterangan tentang keadaan indung telur (folikel de graaf, korpus luteum, korpus albikan), keadaan tuba fallpoii (perlekatan/normal), keadaan peritoneum, rahim, dan sekitarnya.
-
Pemeriksaan ultrasonografi Terutama vaginal ultrasonografi, dilakukan pada saat ovulasi dan didahului dengan pemberian obat dengan klimofen sitral atau perangsang indung telur lainnya.
-
Pemeriksaan uji pasca senggama Untuk mengetahui kemampuan tembus spermatozoa terhadap lendir serviks, caranya dengan melakukan hubungan seks di rumah dan setelah 2 jam, ke rumah sakit untuk pemeriksaan, lendir serviks diambil selanjutnya dilakukan pemeriksaan jumlah spermatozoa yg dijumpai di lendir tsb. Dilakukan pada hari ke 12,13,14 dengan perhitungan menstruasi pertama dianggap hari pertama.
-
Pemeriksaan hormonal Setelah semua pemeriksaan dilakukan dan belum mendapat sebabnya, dapat dilakukan dengan pemeriksaan hormonal. Hormon yg diperiksa adalah FSH, LH, estrogen, prolaktin, progesteron. (Memahami kesehatan reproduksi wanita, Ida Bagus)
13. Bagaimana cara mendiagnosis infertilitas ? 14. Bagaimana penanganan infertilitas pada pria maupun wanita? - Infertilitas dengan penyebab idiopatik Sulit dipecahkan dengan memuaskan. Dalam situasi ini, keyakinan terhadap kebesaran Tuhan sangat terasa sehingga ada baiknya
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
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disamping berobat disertai dengan doa yg tulus dengan permohonan agar diberikan kesempatan untuk memelihara bayi. -
Gangguan Hormonal Pengobatan dengan hormonal bervariasi tergantung dimana letak gangguan hormonnya. Bila gangguan pada proses ovulasi maka pengobatannya dengan induksi ovulasi atau klimofen sitrat. Faktor tingginya prolaktin diobati dengan bromokriptin atau parlodel. Ganguuan
atau
kurangnya
progesteron
dapat
diobati
dengan
menambah progesteron atau sejenisnya. - Kelainan terletak di tuba Kelainan tuba oleh karena infeksi yang menimbulkan gangguan fungsi dapat diselesaikan dengan bedah rekonstruksi tuba. Pemecahan kegagalan fungsi tuba dapat diselesaikan dengan rekayasa canggih assisted fertilization invitro (bayi tabung). 15. Definisi infertilitas? Merupakan masalah yang dihadapi oleh pasangan suami istri yang telah menikah selama minimal satu tahun, melakukan hubungan senggama teratur,
tanpa
menggunakan
kontrasepsi,
tetapi
memperoleh kehamilan. (Ilmu Kandungan, Sarwono) 16. Bagaimana mekanisme terjadinya infertilitas pada laki?
“Knowing is not enough; we must apply. Willing is not enough; we must do.”
belum
berhasil