Pengertian Antenatal Care

Antenatal care adalah pengawasan kehamilan untuk mengetahui kesehatan umum ibu,
menegakan secara dini penyakit yang menyertai kehamilan, menegakan secara dini komplikasi
kehamilan, dan menetapkan resiko kehamilan (Manuaba, 2009).
Tujuan Antenatal Care
Menurut Sondakh (2009) ada beberapa tujuan pemeriksaan ibu hamil secara keseluruhan yaitu:
1. Memantau kemajuan kehamilan untuk mamastikan kehamilan ibu dan tumbuh kembang
janin.
2. Meningkatkan dan mempertahankan kesehatan fisik, mental, social ibu.
3. Mengenali dan mengurangi secara didni adanya penyulit atau komplikasi yang mungkin
terjadi selama hamil, termasuk riwayat penyakit secara umum,dan pembedahan.
4. Mempersiapkan persalinan cukup bulan dan persalinan yang aman dengan trauma
seminimal mungkin.
5. Mempersiapkan ibu agar masa nifas berjalan normal dan mempersiapkan ibu agar dapat
memberikan air susu ibu (ASI) secara ekslusif.
6. Mempersiapkan peran ibu dan keluarga dalam menerima kelahiran janin agar dapat
tumbuh kembang secara normal.
7. Mengurangi bayi lahir prematur, kelahiran mati dan kematiana neonatal, sedangkan
8. Mempersiapkan kesehatan yang optimal bagi janin.

Manfaat Antenatal Care

Manfaat pemeriksaan kehamilan secara dini adalah untuk memperoleh gambaran dasar mengenai
perubahan fisiologik yang terjadi selama kehamilan dan berbagai kelainan yang menyertai
kehamilan secara dini, sehingga dapat diperhitungkan dan dipersiapkan langkah-langkah dalam
pertolongan persalinannya (Manuaba, 2009).
Standar Pelayanan Antenatal Care
1. Frekwensi Antenatal Care

Kunjungan ibu hamil adalah kontak antara ibu hamil dan petugas kesehatan yang memberi
pelayanan antenatal untuk mendapatkan pemeriksaan kehamilan. Menurut Dep Kes RI (2003)
dalam pelaksanaan ANC terdapat kesepakatan adanya standar adanya minimal yaitu dengan
pemeriksaan ANC 4 kali selama kehamilan sebagai berikut : 1). Minimal satu kali pada trimester
I ( 0-13 minggu) 2). Minimal satu kali pada trimester II (14-28minggu) 3). Minimal dua kali
pada trimester III (29-36 minggu).

2. Cakupan Antenatal Care

Cakupan pelayanan Antenatal care dapat di pantau melalui kunjungan baru ibu hamil kunjungan
pertama (K1) atau disebut juga akses dan pelayanan ibu hamil sesuai standar paling sedikit
empat kali dengan distribusi sekali pada triwulan pertama, sekali triwulan kedua, dan dua kali
pada triwulan ketiga dan keempat untuk melihat kwalitas. Cakupan kunjungan ibu hamil
keempat (K4) adalah cakupan ibu hamil yang telah memperoleh pelayanan antenatal care 4 kali
sesuai standar disatu wilayah kerja pada kurun waktu tertentu. Pemerintah menetapkan cakupan
ANC > 95% (Peranginangin, 2006).
3. Pelayanan Anatenatal Care
Menurut Ari, (2009) bahwa dalam penerapan praktek sering dipakai standart minimal pelayanan
antenatal care yang disebut 7T yaitu: (Timbang) berat badan dan tinggi badan, Ukur (Tekanan)
darah. Ukur (Tinggi) fundus uteri, Pemberian imunisasi TT lengkap, Pemberian Tablet zat besi
minimum 90 tablet selama hamil, Tes terhadap penyakit seksual menular, Temu wicara dan
konseling dalam rangka rujukan.
Pelaksanaan Antenatal Care
Menurut Kusmiyati, Wahyuningsi,& Sujiyatini (2008) bahwa pemeriksaan yang sering dilakukan
dirumah sakit atau puskesmas yaitu:
a. Inspeksi
1. Muka : adalah kloasma gravidarum, keadaan selaput mata pucat atau merah, udem, lidah
dan gigi.
2. Leher: apakah ada bendungan vena di leher, kelenjar gondok membesar atau kelenjar
limfe membengkak.
3. Dada : bentuk buah dada, pigmentasi putting susu dan gelanggang susu, keadaan putting
susu, kolustrum.
4. Perut : Perut membesar ke depan atau ke samping, keadaan pusat, pigmentasi linea alba,
nampakkah gerakan anak atau kontraksi rahim, adakah striae gravidarum atau bekas luka

5. Vulva : keadaan perineum, varises, tanda Chadwick, kondylomata, fluor.

6. Anggota bawah : adalah varises, edema, luka dan sikatris pada lipatan paha
b. Palpasi
1. Untuk menentukan besarnya rahim, konsistensinya
2. Bagian-bagian janin, letak, presentasi
3. Gerakan janin

Cara palpasi menurut Leopold (Prawiroharjo & Wiknjosastro, 2005) yaitu:

1. Leopold I Tujuan untuk menentukan tinggi fundud uteri dan untuk menemukan presentasi dengan cara mengidentifikasi bagian tubuh fetus apa yang berada di fundus.
2. Leopold II Tujuan untuk menentukan batas samping rahim kiri-kanan dan untuk
menentukan letak punggung janin dan letak bagian-bagian kecil.
3. Leopold III Tujuan untuk menentukan bagian terbawah sudah atau belum terpegang pada
pintu atas panggul
4. Leopold IV Tujuan untuk menentukan bagian terbawah janin apa dan berapa jauh janin
sudah masuk pintu atas panggul.

c. Auskultasi
Uliyah dan Hidayat (2008) mengindikasikan bahwa auskultasi dilakukan menggunakan
stetoskop monoaural untuk mendengarkan:
1. Denyut jantung janin
2. Bising tali pusat, bising rahim, bising usus
3. Gerakan dan tendangan janin

Daftar Pustaka

Departemen Kesehatan RI. (2003) Pedoman Pelayanan Antenatal di Tingkat Pelayanan

Dasar, Depkes RI, Jakarta.

Kusmiyati, Y., Wahyuningsi, H. P., Sujiyatini., (2008). Perawatan Ibu Hamil. Fitramaya,
Yogyakarta.

Manuaba, I.C., Manuaba, I.B.F., & Manuaba, I.B.G. (2009). Buku Ajar Patologi
Obstetri, EGC, Jakarta.

Prawirohardjo, S. & Wiknjosastro, H. (2005). Ilmu Kebidanan, Yayasan Bina Pustaka,

Jakarta.

Sondakh, N. (2009). Pemeriksaan Antenatal Ibu Hamil, http://mdopost.com

Uliyah, M. & Hidayat, A. (2008). Ketrampilan dasar praktik klinik untuk kebidanan
edisi 2, Salemba Medika, Jakarta.

Definisi Bayi Berat Badan Lahir Rendah

Bayi dengan berat badan lahir rendah (BBLR) adalah neonatus dengan berat badan
lahir pada saat kelahiran kurang dari 2.500 gram (sampai 2.499 gram). BBLR adalah
bayi yang lahir dengan berat lahir kurang 2.500 gram tanpa memandang masa
kehamilan (Prawirohardjo,2008). Dahulu neonatus dengan
berat kelahiran kurang dari 2500 gram atau sama dengan 2500 disebut prematur.
Pada tahun 1961 menurut WHO semua bayi baru lahir dengan berat lahir kurang
dari 2500 gram disebut Low Birth Weight Infant. Hal ini dilakukan karena tidak
semua bayi berat kurang dari 2500 gram pada waktu lahir bayi prematur.
Klasifikasi berat badan bayi baru lahir dapat dibedakan atas (Manuaba, 2007):
a. Bayi dengan berat badan normal, 2.500-4.000 gram
b. Bayi dengan berat badan lebih, lebih 4.000 gram
c. Bayi dengan berat badan rendah, kurang dari 2.500 gram / 1.500-2.500 gram
d. Bayi dengan berat badan sangat rendah, kurang dari 1.500 gram
e. Bayi dengan berat badan ekstrim rendah, kurang dari 1.000 gram

Thrifty Gene Hypothesis:

The thrifty gene hypothesis states that connections between low quality fetal and infant growth
followed by diabetes mellitus type 2 and metabolic syndrome caused by poor nutrition during
early childhood, produces permanent effects in glucose-insulin metabolism.[1] The hypothesis
was proposed by geneticist James V. Neel in 1962 to resolve a fundamental problem. Diabetes is
clearly a very harmful medical condition. Yet it is quite common, and it was already evident to
Neel that it likely had a strong genetic basis. The problem is to understand how disease with a
likely genetic component and with such negative effects may have been favoured by the process
of natural selection. Neel suggested the resolution to this problem is that genes which predispose
to diabetes (called 'thrifty genes') were historically advantageous, but they became detrimental in
the modern world. In his words they were "rendered detrimental by 'progress'". Neel's primary
interest was in diabetes, but the idea was soon expanded to also encompass obesity. Thrifty genes
are genes which enable individuals to efficiently collect and process food to deposit fat during
periods of food abundance.
According to the hypothesis, the 'thrifty' genotype would have been advantageous for huntergatherer populations, especially child-bearing women, because it would allow them to fatten
more quickly during times of abundance. Fatter individuals carrying the thrifty genes would thus
better survive times of food scarcity. However, in modern societies with a constant abundance of
food, this genotype efficiently prepares individuals for a famine that never comes. The result of
this mismatch between the environment in which the brain evolved and the environment of today
is a widespread chronic obesity and related health problems like diabetes.
The hypothesis has received various criticisms and several modified or alternative hypotheses
have been proposed.
Hypothesis and research by Neel
James Neel, a professor of Human Genetics at the University of Michigan Medical School,
proposed the "thrifty genotype" hypothesis in 1962 in his paper "Diabetes Mellitus: A 'Thrifty'
Genotype Rendered Detrimental by 'Progress'?" Neel intended the paper to provoke further
contemplation and research on the possible evolutionary and genetic causes of diabetes among
populations that had only recently come into regular contact with Westerners.[2]
The genetic paradox Neel sought to address was this: diabetes conferred a significant
reproductive (and thus evolutionary) disadvantage to anyone who had it; yet the populations
Neel studied had diabetes in such high frequencies that a genetic predisposition to develop
diabetes seemed plausible. Neel sought to unravel the mystery of why genes that promote

diabetes had not been naturally-selected out of the population's gene pool.[3]
Neel proposed that a genetic predisposition to develop diabetes was adaptive to the feast and
famine cycles of paleolithic human existence, allowing humans to fatten rapidly and profoundly
during times of feast in order that they might better survive during times of famine. This would
have been advantageous then but not in the current environment.[4]
The hypothesis was proposed before there was a clear distinction between the different types of
diabetes. Neel later stated that the hypothesis applied to non-insulin-dependent diabetes mellitus.
In its original form the theory more specifically stated that diabetes may be due to a rapid insulin
response which would prevent loss of glucose from the urine. Furthermore, it made use of a then
popular theory which was later disproven. This argued that specific insulin antagonists were
released in response to insulin with this causing diabetes.[5]
In the decades following the publications of his first paper on the "thrifty genotype" hypothesis,
Neel researched the frequency of diabetes and (increasingly) obesity in a number of other
populations and sought out observations that might disprove or discount his "thrifty gene"
hypothesis.
Neel's further investigations cast doubt on the "thrifty genotype" hypothesis. If a propensity to
develop diabetes were an evolutionary adaptation, then diabetes would have been a disease of
long standing in those populations currently experiencing a high frequency of diabetes. However,
Neel found no evidence of diabetes among these populations earlier in the century.[6] And when
he tested younger members of these populations for glucose intolerance - which might have
indicated a predisposition for diabetes - he found none.[7]
In 1989, Neel published a review of his further research based on the "thrifty genotype"
hypothesis and in the Introduction noted the following: "The data on which that (rather soft)
hypothesis was based has now largely collapsed." However, Neel argued that "...the concept of a
"thrifty genotype" remains as viable as when first advanced...". He went on to advance that the
thrifty genotype concept be thought of in the context of a "compromised" genotype that affects
several other metabolically-related diseases.[8]
Neel in a 1998 review described an expanded form of the original hypothesis, diabetes being
caused by "thrifty genes" adapted specifically for intermittent starvation, to a more complex
theory of several related diseases such as diabetes, obesity, and hypertension (see also metabolic
syndrome) being caused by physiological systems adapted for an older environment being
pushed beyond their limits by environmental changes. Thus, one possible remedy for these
diseases is changing diet and exercise activity to more closely reflect that of the ancestral
environment.[9]
Other research, The thrifty genotype hypothesis has been used to explain high, and rapidly
escalating, levels of obesity and diabetes among groups newly introduced to western diets and
environments, from South Pacific Islanders,[10] to Sub Saharan Africans,[11] to Native
Americans in the Southwestern United States,[12] to Inuit.[13]
The original "thrifty gene" hypothesis argued that famines were common and severe enough to
select for thrifty gene in the 2.5 million years of human paleolithic history. This assumption is
criticized by some anthropological evidence.[14][15][16][17] Many of the populations that later
developed high rates of obesity and diabetes appeared to have no discernible history of famine or
starvation (for example, Pacific Islanders whose "tropical-equatorial islands had luxuriant

vegetation all year round and were surrounded by lukewarm waters full of fish.").[15][16]
Moreover, one of the most significant problems for the 'thrifty gene' idea is that it predicts that
modern hunter gatherers should get fat in the periods between famines. Yet data on the body
mass index of hunter-gatherer and subsistence agriculturalists clearly show that between famines
they do not deposit large fat stores[17]
As a response to such criticisms, a modified "thrifty" gene hypothesis is that the famines and
seasonal shortages of food that occurred only during the agricultural period may have exerted
enough pressure to select for "thrifty" genes.[18]
Thrifty phenotype hypothesis
The thrifty phenotype hypothesis arose from challenges posed to the thrifty gene hypothesis. The
thrifty phenotype hypothesis theorizes that instead of the "thrifty factors" arising from genetic
factors, that instead it is a direct result of the environment within the womb during development.
The development of insulin resistance is theorized to be directly related to the body "predicting"
a life of starvation for the developing fetus.[19]
Hence, one of the main causes of type 2 diabetes has been attributed to poor fetal and infant
growth and the subsequent development of the metabolic syndrome. Since the hypothesis was
proposed, many studies world-wide have confirmed the initial epidemiological evidence.
Although the relationship with insulin resistance is clear at all ages studied, the relation of insulin
secretion is less clear. The relative contribution of genes and environment to these relationships
remains a matter of debate.[20]
Other relevant observations arose from metabolism researchers who note that for practically
every other species on earth, fat metabolism is well regulated[21] and that "most wild animals
are in fact very lean" and that they remain lean "even when adequate food is supplied."
Other alternative hypotheses, In response to the criticisms of the original thrifty genotype theory,
several new ideas have been proposed for explaining the evolutionary bases of obesity and
related diseases.
The "thrifty epigenomic hypothesis" is a combination of the thrifty phenotype and thrifty
genotype hypotheses. While it argues that there is an ancient, canalized (genetically coded)
physiological system for being "thrifty", the theory argues that an individual's disease risk is
primarily determined by epigenetic events. Subtle, epigenetic modifications at many genomic
loci (gene regulatory networks) alter the shape of the canal in response to environmental
influences and thereby establish a predisposition for complex diseases such as metabolic
syndrome. There may be epigenetic inheritance of disease risk.[22]
Milind G Watve and Chittaranjan S Yajnik suggested that changing insulin resistance mediates
two phenotypic transitions: a transition in reproductive strategy from "r" (large number of illnurtured offspring) to "K" (smaller number of carefully nurtured offspring) (see r/K selection
theory); and a switch from a lifestyle dependent upon muscular strength to one dependent on
brain power. Because the environmental conditions that would facilitate each transition are
heavily overlapping, the scientists surmise, a common switch could have evolved for the two
transitions.[19]
An alternative idea to explain the greater prevalence of diabetes in more northerly populations

was suggested by Moalem et al. who noted that recent animal research has uncovered the
importance of the generation of elevated levels of glucose, glycerol and other sugar derivatives
as a physiological means for cold adaptation. High concentrations of these substances depress the
freezing point of body fluids and prevent the formation of ice crystals in cells through
supercooling, thus acting as a cryoprotectant or antifreeze for vital organs as well as in their
muscle tissue. They consequently suggested that factors predisposing to elevated levels of
glucose, glycerol and other sugar derivatives may have been selected for, in part, as adaptive
measures in exceedingly cold climates. The authors suggest that this cryoprotective adaptation
would have protected ancestral northern Europeans from the effects of suddenly increasingly
colder climates, such as those believed to have arisen around 14,000 years ago and culminating
in the Younger Dryas.[23]
Another alternative to the thrifty gene hypothesis is the drifty gene hypothesis proposed by the
British biologist John Speakman. The main feature of this idea is that the current pattern of
obesity does not suggest that obesity have been under strong positive selection for a protracted
period of time. It is argued instead that the obesity comes about because of genetic drift in the
genes controlling the upper limit on our body fatness. Such drift may have started because
around 2 million years ago ancestral humans effectively removed the risk from predators, which
was probably a key factor selecting against fatness. The drifty gene hypothesis was presented as
part of a presidential debate at the 2007 Obesity Society meeting in New Orleans, with the
counter-arguments favouring the thrifty gene presented by British nutritionist Andrew Prentice.
The main thrust of Prentice's argument against the drifty gene idea is that Speakman's critique of
the thrifty gene hypothesis ignores the huge impact that famines have on fertility. It is argued by
Prentice that famine may actually have only been a force driving evolution of thrifty genes for
the past 15,000 years or so (since the invention of agriculture), but because famines exert effects
on both survival and fertility the selection pressure may have been sufficient even over such a
short timescale to generate a pressure for "thrifty" genes. These alternative arguments were
published in two back-to-back papers in the International Journal of Obesity in November 2008.
[18][24]

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