This document provides information on gestational trophoblastic diseases (GTDs), which include a heterogeneous group of lesions arising from abnormal placental trophoblast proliferation. It discusses the classification, epidemiology, pathogenesis, clinical features, diagnosis, and management of GTDs. Key points include: GTDs can be premalignant or malignant (gestational trophoblastic neoplasia/GTN); common premalignant types are complete and partial hydatidiform moles; GTN has varying potential for local invasion and metastasis; combination chemotherapy is recommended for high-risk GTN while single agent chemotherapy is used for low-risk GTN; long-term beta-hCG monitoring is important for follow-up.
gestational trophoblastic disease is discussed in its basic knowledge update to enable undergraduate students help understand the disease, diagnose and treat GTD. also enables to follow and detect complications and malignant transformation of molar pregnancy. single drug and multiple dose chemotherapy depending on staging of the disease and related complications & side effects discussed.
16-Aug-2021-"Gestational trophoblastic disease (GTD) is a spectrum of abnormal growth and proliferation of the trophoblasts of the placenta that continue even beyond the end of pregnancy of the placenta".
gestational trophoblastic disease is discussed in its basic knowledge update to enable undergraduate students help understand the disease, diagnose and treat GTD. also enables to follow and detect complications and malignant transformation of molar pregnancy. single drug and multiple dose chemotherapy depending on staging of the disease and related complications & side effects discussed.
16-Aug-2021-"Gestational trophoblastic disease (GTD) is a spectrum of abnormal growth and proliferation of the trophoblasts of the placenta that continue even beyond the end of pregnancy of the placenta".
Gestational trophoblastic disease (GTD) is a group of pregnancy-related conditions that develop inside a woman's uterus (womb). The abnormal cells start in the tissue that would normally become the placenta. The placenta is the organ that develops during pregnancy to feed the fetus.
Gestational trophoblastic disease (GTD) is a group of rare diseases in which abnormal trophoblast cells grow inside the uterus after conception. In gestational trophoblastic disease (GTD), a tumor develops inside the uterus from tissue that forms after conception (the joining of sperm and egg).
Gestational trophoblastic disease (GTD) is a group of pregnancy-related conditions that develop inside a woman's uterus (womb). The abnormal cells start in the tissue that would normally become the placenta. The placenta is the organ that develops during pregnancy to feed the fetus.
Gestational trophoblastic disease (GTD) is a group of rare diseases in which abnormal trophoblast cells grow inside the uterus after conception. In gestational trophoblastic disease (GTD), a tumor develops inside the uterus from tissue that forms after conception (the joining of sperm and egg).
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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3. Introduction
Gestational Trophoblastic diseases- heterogeneous
group of interrelated lesions that arise from abnormal
proliferation of placental trophoblast.
GTN-subset of malignancies that have varying
propensities for local invasion & mets
GTN-rare human tumors, cured even in the presence
of widespread dissemination
4. WHO Classification
GTD
Premalignant Diseases
Complete Hydatidiform Mole ( C M )
• Partial Hyadatidiform Mole ( P M )
Malignant Diseases (Gestational Trophoblastic Neoplasia)
Nonmetastatic
• Invasive Mole
• Placental site trophoblastic tumor ( PSTT )
• Epitheloid tumour
• Metastatic
• Gestational Choriocarcinoma
5.
6. Epidemiology
It is common in oriental countries- Philippines, China,
Indonesia, Japan, India, Central and Latin Americaand Africa.
India- 1 in 400 pregnancies
Calculated Incidence of complete
mole- 1 in 1945 pregnancies
partial mole- 1 in 695 pregnancies
Age -CMs most common at the extremes of reproductive age
The incidence of CM rises fm I:1000 to 1:76; 1:6.5 in subsequent
pregnancies
CM is the most common antecedent to
Chorio CA. But it can occurafterany type of pregnancy 3% after
invasive mole; 16% after CM
7. In the United States,
•1in 600 In Asian countries,
•The rate is 10 times
higher than in Europeand
North America
therapeutic
abortions
•1 in 1,500
pregnancies
In Saudi Arabia;,
•1.48 in 1000 live births
(hospital-based study;
Felemban AA, et al; 1969)
11. GENETICS
P57 cycline dependent kinase inhibitor paternally
imprinted gene which is maternally expressed
P57 kip2 immunostaining is negative in CM in contrast
to PMs Hydropic abortions & normal placenta
Abnormal Methylation
In cases of Familial recurrent molar pregnancy;
Defective
locus at 19q 13.4 at single gene NALP7 , it is member of
CATERPILLAR family involved in inf lammation &
Apoptosis in genetic CM
Three other genes H19, P57, IGF-2
Chorio CA-specific genes deletion 7p12-q11.2;
Amplification of 7q21-q31 region ; loss of 8p12-p21
12. CLINICAL FEATURES
Complete Mole
Vaginal bleeding
Uterus is larger than POG
Hyperemesis Gravidarum
PET 10-15%
hyperthyroidism 7%
Theca leutin cysts
Beta h CG levels >>
Passage of grapes like vesicle
14. High Risk For Developing Post molar tumor
hCG Levels > 100,000 mIU/L
Excessive Uterine Enlargement
Theca leutin cyst 6cm or larger
15. Clinical features
PARTIALMOLE
Uterus is often not enlarged more than POG
More often presents as Missed or incomplete
abortion
Pre evacuation h CG levels are not more than
100,000IU/ L
Macroscopic : villous swelling is less
intense
Embryo is present
16. Management of Molar Pregnancy
Suction Curettage
Cervical preparation with prostaglandins or
misoprostol should be avoided to reduce the risk
of embolisation.
17. Anti-D Prophylaxis (RCOG)
NOT required in Complete Mole: becauseof poor
vascularisationof the chorionicvilli and absenceof the
D-antigen.
Required in:
-partial mole: due to presence of RBCs
-complete mole: if diagnosis is notconfirmed
histopathologically.
18. Second uterine evacuation
There is NO clinical indication for the routine use
of second uterine evacuation.
It may be useful for symptom control in
selected
patients with heav y bleeding or curative if the
recurrent molar tissue is confined to the uterine
cavity
19. FOLLOW UP
HCG:
weekly determination
of B-HCG until these levels
are normal for 3 consecutive
weeks,folld by monthly values
until normal for 6 consecutive
months
Average time for first normal
HCG post evacuation is 9 weeks,
non detectable HCG levels-risk of GTN is 0
20. Contraception
Should NOT conceive until follow up is complete.
Use Barrier method until hCG revert to normal
(?OCPs may act as growth factor for trophoblastic
tissue).
Once h CG has normalised, the combined oral
contraceptive pill may be used.
IUCD should not be used until hCG levels are
normal to reduce the risk of uterine perforation.
21. Role of prophylactic chemotherapy
The long term prognosis for women with a H. Mole is
not improved with prophylactic chemotherapy.
Because toxicity- including death- may be significant,
it is not recommended routinely (ACOG 2004).
It may be useful in the high-risk cases when
follow upare unavailableorunreliable.
HIGH RISK FACTORS:
. hCG level >100,000 mIU/ml
. Excessive uterineenlargement
. Theca lutiencysts 6 cm in diameter
22. Role of hysterectomy
If the patient desires surgical sterilization, a
hysterectomy may be performed with the mole in
situ.
Hysterectomy does not prevent metastasis;
therefore, patients will require follow up with
assessment of hCG levels.
The ovaries may be preserved at the time of
surgery, even in the presence of prominent theca
luiten cysts.
23. Gestational trophoplastic Neoplasia
Nonmetastatic
Invasive Mole:
Clinical features
Clinical diagnosis by persistence or rising titers of Beta h CG in the
weeks
after molar evacuation & USG
Persistent bleeding p/v
Lower abdominal pain due to invasion in myometrium, vulva, vagina or
intraabdominal metastasis
It may spread to adjacent pervic structures bladder , rectum;
hematuria,
bleeding P/ R
Pulmonary metastasis
Mostly due to initial diagnosis of CM is missed & not on Beta h CG follow
up
25. Clinical features
Placental Site Trophoblastic Tumor (PSTT):
rare slow growing tumor
menstrual irregularities & lower abdominal pain, galactorrhea due to
hyperprolactinemia increased h PL
Little or no h CG is produced ( Free B hCG fragment )
Rarely presents as nephrotic syndrome, hematuria or DIC
Spread is late local Infiltration & metastasis is through lymphatic
Microscopically: In the normal placenta it is distinct from villous
trophoblast & infiltrates thedecidua, myometrium, & spiral arteries.
Mainly from intermediate trophoblast derived fm cytotrophoblast
26. Metastatic Gestational Trophoblastic
Neoplasia
GTN arises when the normal regulatory mechanisms controlling
the proliferation and invasiveness of trophoblastic tissue are
lost.
Diagnosis of the GTN is made on
Clinical presentation
Elevated b-HCG
Evidence of metastasis
Imaging
Tissue for Histology
27. Metastatic Gestational Trophoblastic Neoplasia
CHORIOCARCINOMA:
Clinical features
Occurs mainly following any form
of pregnancy, mainly
after CM
Clinical features of bleeding p/v , lower abdominal pain,
or in 1/3 of cases no pelvic symptoms but symptoms of
distant metastasis lungs , brain ,liver, skin, cauda equina &
the heart may present
Highly malignant , appears as soft purple largely
hemorrhagic mass
28. Microscopic: implanting blastocyst with central cores
of
mononuclear cytotropho surrounded by rim of
multinucleated syncytiotrophoblast & distinct absence of
chorionicvilli extensive areas of necrosis & haemorrage
&frequentevidence of tumor in the sinuses
The hypervascularity & absence of connective
tissue
support are the reason for its highly malignant
behaviour
DIAGNOSIS IS BY BETA h CG
29. investigations
Quantitative beta hCG
X Ray Chest
Pelvic Doppler USG
Abdominal doppler USG to rule out liver & renal metastasis
CT chest , abdomen
MRI brain
Beta h CG in cerebrospinal f luid
PET
Genetic studies
30. FIGO REQUIREMENT FOR MAKING DIAGNOSIS
OF GTN
1. Four values or more of plateaue hCG over at
least 3 weeks: days 1, 7, 14 and 21.
2. A rise of hCG of 10% or greater for 3 values or
more over at least 2 weeks: days 1, 7, and 14.
3. Histologic diagnosis of choriocarcinoma.
4. Persistence of hCG beyond 6 months after
mole evacuation.
31. Metastatic disease
Sites: Symptoms:
a. Pulmonary- Chest pain, dyspnoea
80%
b. Vagina- 30% Vagina bleeding , purulent
discharge and nodule.
c. Liver- 10% Epigastric pain, jaundice,
hepatic rupture leading to
intraperitoneal haemorrhage.
d. Brain- 10% Focal neurological deficit.
32. ANATOMIC FIGO STAGING SYSTEM FOR GTN (2000)
Stage Criteria
I. Disease confined to the uterus
II. Disease outside of uterus but is limited to
the genital structures
III. Disease extends to the lungs with orwithout
known genital tract involvement
IV. All other metastatic sites
33. FIGO prognostic score (2000)
O 1 2 4
Age (years) <39 >39
Antecedent
pregnancy
Hydatidi form
mole
Abortion Term
pregnancy
Interval from index
pregnancy, months
< 4 4-6
103-104
5 cm
7-12 > 12
Pretreatment hCG
(mlU/ml)
< 103 > 104-105 > 105
Largest tumour size,
including uterus
3-4 cm
Site of metastases Spleen,
kidney
GI tract
Single
Brain, liver
Previous failed
chemotherapy
Two or more
drugs
Low risk (Score 0-6) and high risk (score> 7)
35. Low Risk GTN
FIGO score 6 or less.
Drugs schedules: single agent chemotherapy
Most commonly used regimen.
Methotrexate: 1 mg/kg 1M on days 1, 3, 5, 7
Folinic acid 0.1 mg/kg 1M on days, 2, 4, 6 and 8.
Side Effects: Stomatitis, conjunctivitis, abdominal and
chest pain.
Actinomycin- D: (primary therapy in case of abnormal
liver function)
36. After the first treatment
Further chemotherapy is withheld as long as the
HCG level is falling progressively
Additional single agent chemotherapy is
not
administered at any predetermined or fixed
interval
II courseof CT if:
If HCG level plateaus for more than 3 consecutive
weeks or begins to rise again
If HCG level does not decline by 1 log within 18
days of completion of first treatment
If response to first treatment was inadequate,dose
of
MTX is increased from 1mg/kg/day to 1.5 mg/kg/day
for each of the 4 treatment days
37. Role of hysterectomy in non metastatic
disease i.e. Stage-I
If patient does not wish to preserve fertility
hysterectomy with adjuvant single agent
chemotherapy given.
In case of stage-I PSTT.
Role of adjuvant chemotherapy.
1. Decrease dissemination of viable tumor cells at
surgery.
2. Maintain cytotoxic level of chem.
3. To treat any occult metastasis
38. Follow up in Low risk GTN
Weekly bhCG titre until normal for 3 consecutive
weeks.
Monthly b HCG level until normal for 12 consecutive
months.
Effective contraception during the follow
up
FIGO recommends additional 2 courses of
chemotherapy after initial negative b hCG.
39. High Risk GTN
Stage I, II, III With FIGO score 7 or greater or Stage IV
Primary intensive combination chemotherapy
Regimes given :
. MAC.
. Modified Bagshawe (CHAMOCA)
. EMA-CO
. EMA-EP.
40. MAC-III Regime
Mtx 1 mg/kg IM/1V Days 1, 3, 5, 7
Folinic acid
Actinomycin-D
0.1 mg/kg IM Days 2, 4, 6, 8
Days 1-5
12 g/kg IV
Cyclophosphamide 3 mg/kg IV Days 1-5
To be repeated every 15 days if toxicity permits.
41. EMA-CO Regime
Etoposide, methotrexate, actinomycin D, alternating weekly with
cyclophosphamide and oncovin.
Day 1 Actinomycin D 500 micrograms IV push
IV. Etoposide 100 mg/m2 over 30-50 min.
Methotrexate 100 mg/m2 IV infusion over 1
hr and then
Methotrexate 200 mg/m2 IV infusion over 12 hrs
Day 2
Day 8
Actinomycin D 500 micrograms IV push new IV
Etoposide 100 mg/m2 over 30-50 min.
Folinicacid 15 mg IV push Q 6 hrs for 8 doses
beginning 24 hrs after methotrexate bolus.
Vincristine (Oncovin) 1 mg/m2 IV
Cyclophosphamide 600 mg/m2 IV
SIDE EFFECT:- Myelosuppresion ,Mucositis , Neuropathy ,Reversible
alopecia
42. . EMA-EP
In patient resistant to EMA-CO
On day 8
Etoposide- 10 mg/m2 iv.
Cisplatin- 80 mg/m2 iv
treatment – until 3 consecutive weekly titres
normal.
2-4 cycles given further after initial normal b
H.C.G.
43. Follow up OF High risk GTN
Weekly bHCG until normal for 3
consecutive weeks.
Monthly bHCG for 24 consecutive
months.
Contraception in follow up period.
44. Management of sites of metastasis
VAGINAL &PELVIS -30%
Single agent chemotherapy –Low risk
Combination chemotherapy –High risk
If bleeding occurs-
Vaginal packing
Wide local excision
Arteriographic embolisationof hypogastricarteries
45. PULMONARY-80%
Present as – Chest pain, cough, hemoptysis dyspnoea.
X-ray features- Snowstorm
Discrete round densities.
Pleural effusion
Embolic pattern
Rx
Single agent chemotherapy-low risk.
Combination – high risk.
Thoracotomy-viable pulmonary
Metastasis following comb chemo
46. . HEPATIC-10%
Worse prognosis.
Usually associated with widespread metastasis Intraperitoneal
bleeding may occur.
Rx
Chemo & concurrent
radiation (2000-3000 cGy).
Hepatic resection to excise
resistant foci.
Cerebral-10%
Acute focal neurological
deficits.
Combination chemo + WBRT (2000-3000).
Patients with metastasis on initial evaluation respond better
than who develop Lesion during therapy.
During period of WBRT- Mtx in EMA-CO be increased to 1 g/m2
with Folinic.Acid rescue.
47. For subsequent pregnancy.
Ist trimester TVS to confirm normal pregnancy.
bHCG 6 wks after termination of pregnancy .
After effective treatment for non-malignant GTN molar
pregnancy occur in 1-2% subsequent pregnancies.
48. CASES REGISTERED IN GTD
CLINIC,GRH
Total no of cases-15
Case 1:
Mrs.Kavitha,28 yr old P2L2A2/MTP with TAT done in
FPAI(8.4.15)/C/O bleeding pv/RPOC with secondary
infection/?invasive partial mole(hcg-1247)-GRH admission-
SE 0n 4.5.15-(hcg-141 on 8.5)
Pt was on weekly b-hcg follow up until 3 normal
values,monthly follow up until 6 normal values,
17.02.16-1.02
16.03.16-120.6
Started on methotrexate
50. Case 2:latha 19 yr unmarried/molar pregnancy/SE @
GRH on 12.08.15 for molar/presented with bleeding pv
I mth later with severe anemia/re evacuation done for
retained tissues
In the post molar evacuation surveillance,weekly b-
hcg rising trend-started on single agent CT
EMACO started
52. Case 3:
Mrs,nambuselvi,42 yr old primi/ms 22 yrs/13 wks
GA/partial molar pregnancy/SE done
Pre evacuation B-HCG-1,14,560
Chest x ray-S/O tiny nodular opacity in left
midzone
Pt transferred to med onco in view of invasive mole
Single agent CT-MTX