STEP 7 LBM 4 HERBAL

Apa saja syarat2 untuk menjadi dokter terapis herbal medik?

POWERPOINT
Mengapa timbul gejala mual-mual di pagi hari pada hiperemis
gravidarum?
Hyperemesis gravidarum (HG) is a severe,
debilitating nausea and vomiting in pregnancy that generally leads
to more than 5 percentweight loss and may require fluid and
nutritional supplement. It is different from the more common
nausea and vomiting known asmorning sickness. Hyperemesis is
considered a rare complication of pregnancy but, because nausea
and vomiting during pregnancy exist on a continuum, there is
often not a good diagnosis between common morning sickness
and hyperemesis. Estimates of the percentage of pregnant women
afflicted range from 0.3% to 2%

Morning sickness, also called nausea
gravidarum, nausea, vomiting of pregnancy (emesis
gravidarum or NVP), or pregnancy sickness is a condition that
affects more than half of all pregnant women. Sometimes
symptoms are present in the early hours of the morning and
reduce as the day progresses. However, in spite of its common
name, it can occur at any time of the day. For most women it may
stop around the 12th week of pregnancy.

Related to increased estrogen levels, a similar form of nausea is
also seen in some women who use hormonal
contraception orhormone replacement therapy. The nausea can be
mild or induce actual vomiting, however, not severe enough to
cause metabolic derangement. In more severe cases, vomiting
may cause dehydration, weight loss, alkalosis and hypokalemia.
This condition is known as hyperemesis gravidarum and occurs in
about 1% of all pregnancies. Nausea and vomiting can be one of
the first signs of pregnancy and usually begins around the 6th
week of pregnancy (counting gestational age from 14 days before
conception).
1. ^ Hyperemesis Education & Research Foundation Understanding
Hyperemesis: Overview
2. ^ Eliakim, R., Abulafia, O., & Sherer, D. M. (2000). "Hyperemesis
gravidarum: A current review". American Journal of
Perinatology 17 (4): 207218. doi:10.1055/s-2000-
9424. PMID 11041443.
3. ^ "HG Theories & Research". helpher.org. Retrieved 25 December
2012.
4. ^
a

b

c
Laura Geggel (3 December 2012), A Royal Spotlight on a
Rare Condition The New York Times
5. ^ Basso, O; Olsen, J (2001 Nov). "Sex ratio and twinning in
women with hyperemesis or pre-eclampsia.". Epidemiology
(Cambridge, Mass.) 12 (6): 747-9. PMID 11679806.
6. ^ Hershman JM (June 2004). "Physiological and pathological
aspects of the effect of human chorionic gonadotropin on the
thyroid". Best Pract. Res. Clin. Endocrinol. Metab. 18 (2): 249
65. doi:10.1016/j.beem.2004.03.010. PMID 15157839.






Proximate causes of pregnancy sickness include:
An increase in the circulating level of the hormone estrogen. Estrogen
levels may increase by up to a hundredfold during
pregnancy.
[1][unreliable source]
However, there is no consistent evidence of
differences in estrogen levels and levels of bilirubin between women
that experience sickness and those that do not.
[2]

Low blood sugar (hypoglycemia) due to the placenta's draining
energy from the mother, though studies have not confirmed this.
[3]

An increase in progesterone relaxes the muscles in the uterus, which
prevents early childbirth, but may also relax
the stomach andintestines, leading to excess stomach
acids and gastroesophageal reflux disease.
An increase in human chorionic gonadotropin. It is probably not the
human chorionic gonadotropin itself that causes the nausea. More
likely, it is the human chorionic gonadotropin-stimulating the
maternal ovaries to secrete estrogen, which in turn causes the
nausea.
[4]

An increase in sensitivity to odors, which overstimulates normal
nausea triggers.
An increase in bilirubin levels due to increased liver enzymes.
Note that Gastroesophageal reflux disease can also be caused by
pregnancy, and may result in nausea and vomiting.
Morning sickness is believed to be an evolved trait that protects the
fetus against toxins ingested by the mother.
[5]

[6]
Many plants contain
chemical toxins that serve as a deterrent to being eaten. Adult humans,
like other animals, have defenses against plant toxins, including
extensive arrays of detoxification enzymes manufactured by
the liver and the surface tissues of various other organs. In the fetus,
these defenses are not yet fully developed, and even small doses of
plant toxins that have negligible effects on the adult can be harmful or
lethal to the embryo.
[7]
Pregnancy sickness causes women to experience
nausea when exposed to the smell or taste of foods that are likely to
contain toxins injurious to the fetus, even though they may be harmless
to her.
There is considerable evidence in support of this theory, including:
[8]

[9]

Morning sickness is very common among pregnant women, which
argues in favor of its being a functional adaptation and against the
idea that it is a pathology.
Fetal vulnerability to toxins peaks at around 3 months, which is also
the time of peak susceptibility to morning sickness.
There is a good correlation between toxin concentrations in foods,
and the tastes and odors that cause revulsion.
Women who have no morning sickness are more likely
to miscarry.
[10]
This may be because such women are more likely to
ingest substances that are harmful to the fetus.
[11]

In addition to protecting the fetus, morning sickness may also protect
the mother. Pregnant women's immune systems are suppressed during
pregnancy, it is presumed to reduce the chances of rejecting tissues of
their own offspring.
[12]
Because of this, animal products
containing parasites and harmful bacteria can be especially dangerous to
pregnant women. There is evidence that morning sickness is often
triggered by animal products including meat and fish.
[13]

If morning sickness is a defense mechanism against the ingestion of
toxins, the prescribing of anti-nausea medication to pregnant women
may have the undesired side effect of causing birth defects or
miscarriages by encouraging harmful dietary choices.
[8]
On the other
hand, many domestic vegetables have been purposely bred to have
lower levels of toxins than in the distant past, and so the level of threat
to the embryo may not be as high as it was when the defense
mechanism first evolved.
[14]



1. ^ Hook, E. B. (1976). "Changes in tobacco smoking and ingestion
of alcohol and caffeinated beverages during early pregnancy: are
these consequences, in part, of feto-protective mechanisms
diminishing maternal exposure to embryotoxins?". In Kelly,
S..Birth Defects: Risks and Consequences. Academic Press.
pp. 173181.
2. ^ Profet, Margie (1992). "Pregnancy Sickness as Adaptation: A
Deterrent to Maternal Ingestion of Teratogens". In Barkow,
Jerome; Cosmides; Tooby, Leda. The Adapted Mind: Evolutionary
Psychology and the Generation of Culture. Oxford University
Press. pp. 327365.
3. ^ Beck, F. (1973). Human Embryology and Genetics. Blackwell
Scientific.
4. ^
a

b
Nesse, Randolphe M; Williams, George C (1996). Why We
Get Sick (First ed.). New York: Vintage Books. pp. 290.
5. ^ Pepper, GV; Roberts, Gillian V. (2006). "Rates of nausea and
vomiting in pregnancy and dietary characteristics across
populations". Proceedings of the Royal Society B273 (1601):
2675
2679. doi:10.1098/rsbp.2006.3633. PMC 1635459.PMID 17002954
.
6. ^ Chan, Ronna L. et al.; Olshan, A. F.; Savitz, D. A.; Herring, A.
H.; Daniels, J. L.; Peterson, H. B.; Martin, S. L. (Sept. 22,
2010). "Severity and duration of nausea and vomiting symptoms
in pregnancy and spontaneous abortion". Human
Reproduction25 (11): 2907
12. doi:10.1093/humrep/deq260. PMC 3140259. PMID 20861299.
7. ^ Sherman, Paul W.; Flaxman, Samuel M. (2002). "Nausea and
vomiting of pregnancy in an evolutionary perspective". Am J
Obstet Gynecol 186 (5): S190
S197.doi:10.1067/mob.2002.122593. PMID 12011885.
8. ^ Haig, David (October 1993). "Genetic conflicts in human
pregnancy". Quarterly Review of Biology 68 (4): 495
532. doi:10.1086/418300. PMID 8115596.
9. ^ Flaxman, Samuel M.; Sherman, Paul W. (June 2000). "Morning
sickness: a mechanism for protecting mother and
embryo". Quarterly Review of Biology 75 (2): 113
148. doi:10.1086/393377. PMID 10858967.
10. ^ Martin, Mike (June 29, 2009). "Margie Profet's Unfinished
Symphony". Weekly


Mengapa dokter memutuskan untuk memberikan terapi herbal
daripada memberikan terapi konvensional? Apa tujuannya?
Apa saja terapi konvensional untuk hiperemis gravidarum?

While no medication is considered completely risk-free for use during
pregnancy, there are several that are commonly used to treat HG and
are believed to be safe.
The standard treatment in most of the world is pyridoxine/doxylamine ,
(known as Bendectin, or Debendox in the UK and Diclectin in Canada), a
combination ofdoxylamine succinate and pyridoxine (vitamin
B
6
). However, due to a series ofbirth-defect lawsuits in the United
States against its maker, Merrell Dow , Bendectin is not currently on the
market in the U.S. (None of the lawsuits were successful, and numerous
independent studies and the Food and Drug Administration (FDA) have
concluded that Bendectin does not cause birth defects.) Its component
ingredients are available over-the-counter (doxylamine succinate is the
active ingredient in many sleep medications), and some doctors will
recommend this treatment to their patients.
Antiemetic drugs, especially ondansetron (Zofran), are effective in many
women. The major drawback of ondansetron has been its cost. In
severe cases of HG, the Zofran pump may be more effective than
tablets. Zofran is also available in orally disintegrating tablet (ODT)
form, which can be easier for women who have trouble swallowing due
to the nausea. Promethazine(Phenergan) has been shown to be safe, at
least in rats and may be used during pregnancy with minimal/no side-
effects. Metoclopramide is sometimes used in conjunction with
antiemetic drugs; however, it has a somewhat higher incidence of side-
effects. Other medications less commonly used to treat HG
include corticosteroids , and antihistamines .[26] Long term use of
corticosteroids may render pregnant woman more susceptible to
infections.[11]
Other less commonly used treatments are tetrahydrocannabinol (THC)
andmedical cannabis . THC is the principal psychoactive constituent of
the cannabis plant and is available by prescription in the U.S. and
Canada under the brand name Marinol . Marijuana, specifically cannabis
sativa , was found in a 2006 study to have been "extremely effective"
and "effective" in the treatment of symptoms of HG, which is similar to
its effects for people suffering from similar symptoms for other reasons
like chemotherapy .[27] Queen Victoria of the United Kingdom of Great
Britain and Ireland, who is known by many as the first medical
marijuana pharmacologist, used marijuana to treat her worst symptoms
associated with her pregnancies.[28][29] Prenatal maternal use of
marijuana is allegedly child abuse in some jurisdictions,[30] and not in
others.[31] A peer-reviewed published study, albeit with a small sample
size and not reproduced, found no significant differences in
developmental testing outcomes between children of marijuana-using
and non-using mothers except at 30 days of age when the babies of
users had more favourable scores on two clusters of the Brazelton
Scales: autonomic stability and reflexes.[32]
1. ^ In re P.T., 9th Dist. 6293 (Ohio App. 2007).
2. ^ Matter of Jones v. Jones, 50257 (NY: Family Court 2012).
3. ^ Hayes, J. S.; Lampart, R.; Dreher, M. C.; Morgan, L. (1991).
"Five-year follow-up of rural Jamaican children whose mothers
used marijuana during pregnancy". The West Indian medical
journal 40 (3): 120123. PMID 1957518.

Medical Care
Initial management should be conservative and may include
reassurance, dietary recommendations, and support. Alternative
therapies may include acupressure and hypnosis.
[36]

Studies have not shown a clear benefit of acupressure in patients with
hyperemesis gravidarum. However, a randomized study by Rosen et al
using pressure or electrical stimulation at the P6 (or Neguian) point on
the inside of the wrist showed some efficacy in reducing nausea and
vomiting and promoting weight gain in women with hyperemesis
gravidarum.
[37]

More controversy surrounds the benefit of hypnosis, but it has been
studied in some cases of hyperemesis gravidarum and has been shown
to be beneficial.
Psychological counseling may be considered.
[36]

Outpatient or home intravenous hydration should be considered. If
medications and outpatient hydration fail or if severe electrolyte
disturbances persist, inpatient admission for intravenous hydration may
be necessary.
Pharmacologic therapy
If pharmacologic therapy is necessary, treatment may be initiated using
vitamin B-6, 10-25 mg daily, 3-4 times daily; doxylamine, 12.5 mg, 3-4
times daily can be used in addition. The herb, ginger capsules 250 mg 4
times daily, can be added at this point if patient is still vomiting since it
has been shown to be effective in randomized trials.
[38]
Metoclopramide,
5-10 mg taken orally q8h may be used next. Promethazine, 12.5 mg
orally or rectally q4h, or dimenhydrinate 50-100 mg orally q4-6h, may
be added as well. Ondansetron 4-8 mg orally or IV q8h can be used for
further refractory cases. Methylprednisolone, 16 mg orally or IV q8h for
3 days, with a taper to lowest effective dose, can be used if persistent
vomiting occurs despite the above therapy. Steroids seem to increase
risk for oral clefts in first 10 weeks of gestation.
[39, 5]

Metoclopramide is widely used for nausea and vomiting during
pregnancy, but information regarding human teratogenicity has been
lacking. Matok et al found no increased risk for major congenital
malformations, low birth weight, preterm delivery, Apgar scores, or
perinatal death between infants of mothers who took metoclopramide
within the first trimester compared with infants mothers who did not
take metoclopramide. The retrospective cohort study included a total of
81,703 infants who were born to women registered in a single health
system with computerized maternal and infant hospital records. Of
these, 3458 (4.2%) had first trimester exposure to metoclopramide.
[40]

Since confirmation of adherence was unavailable, a secondary analysis
was performed on infants of mothers who refilled their prescription for
metoclopramide at least once (n=758), and no increased risk was found
in this subpopulation exposed to metoclopramide compared with infants
not exposed. Additionally, the results of the study were unchanged
when therapeutic abortions of exposed and unexposed fetuses were
included in the analysis.
The study provides clinicians reassurance that metoclopramide does not
cause congenital malformations; although, dopamine antagonists can
cause maternal extrapyramidal symptoms (ie, acute dystonic reactions,
tardive dyskinesia).
If hypokalemia is severe or symptomatic, potassium should be replaced
parenterally. Before administering intravenous potassium, renal function
should be evaluated. Potassium is usually added to intravenous fluid to
achieve a concentration of 40 mEq/L (and not >80 mEq/L). An infusion
rate of 10 mEq of potassium per hour should be safe as long as urine
output is adequate.
When administrating intravenous hydration to a patient who has severe
volume depletion in an effort to prevent the development of Wernicke
encephalopathy, avoid intravenous glucose until intravenous thiamine
has been administered.
If persistent dehydration, electrolyte loss, and/or weight loss occur
despite above therapy, nutrition supplementation by either the
parenteral or enteral route is indicated. The standard method has been
via total parenteral nutrition (TPN). However, documented risks of
bacteremia, sepsis, and thrombosis have been associated with the PICC
lines required for TPN supplementation. Nasogastric tube placement and
subsequent enteral feeding has been shown in small series and reports
to be a valid alternative, with less complication risks, similar efficacy,
and similar outcomes in regard to neonatal outcome when compared
with TPN.
[41]

http://emedicine.medscape.com/article/254751-treatment




Mekanisme kerja ginger dalam antiemetik

Against nausea and vomiting (antiemetic) during motion
sickness and seasickness (Langner et al., 1998; Stewart et
al., 1991; Grontved et al., 1988; Grontved and
Hentzer,1986; Mowery and Clayson, 1982). Apparently, this
effect is not mediated through the central nervous system
(CNS), but rather, gingers active principles act directly on
the gastrointestinal tract (Foster and Tyler 2000; Holtmann
et al., 1989).
Ginger juice produces antimotion sickness action possibly by
central and peripheral
anticholinergic and antihistaminic effects (Qian and Liu,
1992). Some researchers hypothesize that ginger
ameliorates the nausea associated with motion sickness by
preventing the development of gastric dysrrhythmias and the
elevation of plasma vasopressin (Lien et al., 2003).
To treat hyperemesis gravidarum (serious cases of morning
sickness), especially during the first trimester of pregnancy
(Barrett, 2004; Kraft and Hobbs, 2004; Blumenthal, 2003,
2000, 1998; Fugh-Berman and Kronenburg, 2003; McCann,
2003; Chandra et al., 2002; Ernst and Schmidt, 2002;
Hollyer et al., 2002; Jewell and Young, 2002; Keating et al.,
2002; Maats and Crowther, 2002; Niebyl and Goodwin,
2002; Al-Ari 2001; Power et al., 2001; Tsui et al., 2001;
Wilkinson, 2000; Fischer-Rasmussen, et al., 1990).
To prevent or reduce nausea and vomiting in postoperative
patients (Barrett, 2004; Kraft and Hobbs, 2004; Visalyaputra
et al., 1998; Arfeen et al., 1995; Phillips et al., 1993; Bone et
al., 1990).
To reduce vomiting in patients treated with cytotoxic
compounds (Yamahara et al., 1989).
To stimulate the appetite (Kraft and Hobbs, 2004; Schulz et
al., 2001; Adame and Adame, 2000).
To promote digestion and as an antiflatulent or carminative
to reduce gas and bloating (Lewis and Elvin-Lewis, 2003;
Chevallier, 2000; Ody, 2000).
For temporary relief and protection against gastrointestinal
ulcers (McCann, 2003; Wu et al., 1990)
To improve blood circulation (Chevallier, 2000; Ody, 2000).
To lower blood glucose in the treatment of diabetes (Barnes
et al., 2002; Mascolo et al., 1989).
To lower or increase (depending on the dose) arterial
tension (Barnes et al., 2002).
As an anti-inflammatory against rheumatic pain and arthritis
(Altmann and Marcussen, 2001; Bliddal et al., 2000).
As a mild antipyretic to reduce fever (Ara, 1997).
As a sialagogue, to promote salivation (Wichtl, 2004;
Berdoncs, 1998).
As a diaphoretic, to promote sweating (Chevallier, 2000).
To treat cancer, due to its possible antitumorigenic effects
(McCann, 2003).
As a cholagogue, to promote the flow of bile into the
intestine (Vanaclocha and Canigueral, 2003; Karch, 1999).
To treat migraine headache (Metz and Cupp, 2000).
Against sore throat and minor respiratory ailments
(Gruenwald, 2004; Martinez, 1989).
Ginger root, in large doses, has positive inotropic effects on
the cardiovascular system (Skidmore Roth, 2003).
Topically, ginger preparations have been used for their
antiseptic action (Chevallier, 2000; Ody, 2000).
Apakah ginger aman untuk pengobatan hiperemis gravidarum?
Pregnancy & Lactation
Pregnancy Category: not recommended by German Commission E;
however, current data indicate safe when used at usual therapeutic dose
Lactation: N/A
Pregnancy Categories
A:Generally acceptable. Controlled studies in pregnant women show no
evidence of fetal risk.
B:May be acceptable. Either animal studies show no risk but human
studies not available or animal studies showed minor risks and human
studies done and showed no risk.
C:Use with caution if benefits outweigh risks. Animal studies show risk
and human studies not available or neither animal nor human studies
done.
D:Use in LIFE-THREATENING emergencies when no safer drug
available. Positive evidence of human fetal risk.
X:Do not use in pregnancy. Risks involved outweigh potential benefits.
Safer alternatives exist.
NA:Information not available.
http://reference.medscape.com/drug/african-ginger-black-ginger-
344468
In summary, ginger is a safe and effective treatment option for
nausea and vomiting of pregnancy and comparable with vitamin
B6 in effectiveness. Future research needs to address potential
risks from high doses during pregnancy, but ginger has a long
history of safety, because it has been used for centuries for
medicinal purposes as well as a food substance and spice. The
FDA classies ginger as Generally Recognized as Safe, and the
German Commission E monographs.
Eva Bryer, CNM, MSN, is a recent graduate of the UCSF/SFGH
Interdepartmental Nurse-Midwifery Program, Volume 50, No. 1,
January/February 2005
Safety/Precautions

Ginger is usually regarded as safe in small amounts (Libster, 2003;
Chandra et al., 2002; Ernst and Pittler, 2000; Metz and Cupp, 2000),
although certain precautions should be borne in mind, as follows: High
doses of ginger may have uterine stimulating properties (Castleman,
2001). Do not use in pregnancy or lactation, unless prescribed by a
health professional, as the possible effects on the developing fetus have
not yet been ascertained (McCann, 2003; Ernst and Schmidt, 2002; Al-
Achi, 2001; Arteche and Vanaclocha, 1998). In animal experiments,
ginger has not shown any teratogenic effect when applied during
pregnancy (Weidner and Sigwart, 1998). Curiously, Wilkinson (2001)
found that ginger tea applied orally to rats was not materno-toxic, but
increased fetal loss, although augmenting growth in the surviving
fetuses. In a human study, ginger showed no teratogenic effects
(Fischer-Rasmussen, et al., 1990). In experiments carried out in India,
ginger has not shown any mutagenic activity (Sivaswamy et al., 1991).
Do not use in medicinal doses in patients with gallstones (cholelithiasis),
as gingers cholagogue effect may stimulate the gall bladder, worsening
symptoms and causing unnecessary pain (Skenderi, 2003; Skidmore-
Roth, 2003; Karch, 1999). It has been mentioned that gingers
components may inhibit thromboxane synthesis in vitro, thus interfering
with normal blood clotting (Abebe, 2003; Backon, 1991; Srivastava,
1989). Although the putative anti-thrombotic activity of ginger in humans
has not been proven (Janssen et al.,1996; Lumb, 1994), as a precaution,
suspend the use of this herb two weeks before surgery. (Robbers and
Tyler, 2000). Large doses of ginger may cause cardiac arrhythmia and
CNS depression (Gruenwald 2000), as well as heartburn (Castleman
2001; McCann, 2003). Chinese herbalists differentiate between the use
of fresh and dry ginger root, and suggest using caution in using dry
ginger during pregnancy (Libster, 2003). Ginger overdose may cause
arrhythmias and depression of the central nervous system (Cassileth and
Lucarelli, 2003).

Herb Drug Interactions

Do not use concurrently with other plants or herbal products that may
interfere with normal blood clotting, such as garlic, ginseng or ginkgo,
for example (Abebe, 2002; Brinker, 2001). Do not use concurrently with
drugs that interfere with blood clotting, such as aspirin, heparin or
warfarin (Abebe, 2002; Brinker 2001; Miller, 1998). Patients under
treatment with antiarrythmic drugs or CNS depressants should observe
caution if using ginger preparations (Cassileth and Lucarelli, 2003;
McCann, 2003). Ginger may increase the absorption of other drugs
taken orally (Skidmore-Roth, 2003). Ginger may antagonize activity of
proton pump inhibitors and H2 blockers by means of increased
production of stomach acid (Cassileth and Lucarelli, 2003). If used
against motion sickness, do not combine ginger with other medications
for the same purpose, such as dimenhydrinate (Dramamine), since the
possible interactions are currently unknown. Avoid taking concurrently
with oral hypoglycemics, as Ginger could theoretically potentiate their
effects (Cassileth and Lucarelli, 2003)
http://www.herbalsafety.utep.edu/safety.asp?pk=9

Hal-hal yang harus diperhatikan untuk penggunaan ginger
terhadap ibu hamil di skenario?
Kandungan apa yang terdapat pada ginger sehingga dapat
meredakan morning sickness?

Pharmacology
Metabolism: N/A
Excretion: N/A
Mechanism of Action
Galanolactone: 5HT3 antagonist
Inhibits prostaglandin & eicosanoid synthesis
http://reference.medscape.com/drug/african-ginger-black-ginger-
344468
The rhizomes (underground stems) (Samuelsson, 2000). ***Active
principles The content of the active principles is not uniform and
can vary significantly between plant varieties and regions in which
ginger is grown. (Bruneton, 1999; Foster and Tyler, 2000;
Gruenwald 2000; Robbers and Tyler, 2000). In some instances,
certain commercial preparations made from ginger are devoid of
any medicinal activity, as the plants essential components have
been extracted before packaging (Adame and Adame, 2000).
Volatile oil (zingiberene, zingiberol, D-camphor) Shogaols
Diarylheptanoids (gingerenones, A and B) Gingerols (Skenderi,
2003; Gruenwald, 2000).
http://www.herbalsafety.utep.edu/medical.asp?pk=9

Apa bentuk sediaan ginger untuk mengatasi morning sickness?
POWERPOINT
Jahe jenis apa yang digunakan untuk terapi pada morning sickness
seperti di skenario?
Zingiber ofcinale