This document discusses molar pregnancy, which occurs when abnormal placental tissue develops instead of an embryo. It defines molar pregnancy and describes the classification of gestational trophoblastic disease. It also covers the pathogenesis, risk factors, clinical features, diagnosis, and management of complete and partial molar pregnancies. The key aspects are evacuation of the molar tissue followed by monitoring of hCG levels to detect persistent trophoblastic disease.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
1. MOLAR
PREGNANCY
DR. YOGESH PATEL
MBBS, DGO
DIPLOMA IN LAPAROSCOPY (D. MAS)
FELLOWSHIP IN LAPAROSCOPY (F. MAS)
FELLOWSHIP IN INFERTILITY (F. ART)
PG DIPLOMA IN ULTRASONOGRAPHY (D. USG)
EMERGENCY MEDICINE SPECIALIST
FORMER CONSULTANT AIIMS NEW DELHI
MEMBER OF THE WORLD ASSOCIATION OF LAPROSCOPIC SURGEONS
2.
3. WHAT IS MOLAR PREGNANCY?
⚫A molarpregnancy happenswhen tissue that normally
becomes a fetus instead becomes an abnormal growth
in uterus. Even though it isn't an embryo, this growth
triggers symptomsof pregnancy
DEFINATION:
⚫A heterogeneous group of interrelated lesions arising from
the trophoblastic epithelium of the placenta ,(tropho
means nutrition, blast means early developmental cells)
characterized by adistinct tumor marker –β HCG as tumor
arises from gestational rather than maternal tissue.
4. What is the classification of
gestational trophoblastic
disease?
5. Gestational Trophoblastic Disease (GTD)
It is aspectrumof trophoblasticdiseases that includes:
Hydatiform mole (Benign)
Complete mole
Partial mole
Gestational trophoblastic neoplasia (Malignant)
Invasive mole
Choriocarcinoma
Placental site trophoblastictumour
Epitheloid trophoblastic tumour
The last 3 may follow abortion, ectopic or normal pregnancy
FIGO oncology committee; Williams Obsterics
23rd , 2010
6. It is aspectrumof trophoblasticdiseases thatdevelops
malignantsequelae. GTN includes:
Invasive mole
Choriocarcinoma
Placental site trophoblastictumour
Epitheloid trophoblastic tumour
Gestational Trophoblastic Neoplasia (GTN)
=Malignant Gestational Trophoblastic Disease
Disaia &Creasman Clinical Gynecological Oncology 2007
Cunningham et al Williams Obsterics 23rd , 2010
9. Risk Factors
Age: extremes of age <15 yr and >40 yr
Reproductive history:
Prior Molar Pregnancy
Previous spontaneous abortion: double the incidence
Second molar: 1% - Third molar : 20%!
Diet: increase incidence in high carbohydrate diet, low protein and Vit.A or
carotene diet (complete mole)
Malnutrition and debilitated condition.
Repetitive H. moles in women with different partners
Maternal Blood GroupAB andA
High gamma globin in absence of hepatic disesase
11. In the United States,
1 in 1,500 -2,000
pregnancies
In Asian countries,
•The rate is 10 times
higher than in Europeand
North America
In Saudi Arabia;,
•1.48 in 1000 live births
(hospital-based study;
Felemban AA, etal; 1969)
1 in 200-300 pregnancies in
south eastasia.
1-2 in 1,000 pregnancies in
Chinaand Japan.
Incidence
highest in
philippines i,e
1 in 80
12. WHAT IS THE CHROMOSOMAL
BASIS OF DEVELOPMENT OF
MOLE?
13. Pathogenesis and Cytogenetics of HM
Genetic
Constitution
Diploid Triploid/ teraploid
Patho-genesis
4%
Fertilization
of an empty
ovum by two
sperms
“Diandric
dispermy”
90%
Triploid
fertilization of
a normal
ovum by two
sperms
“Dispermic
triploidy”
96%
Fertilization
of an empty
ovum by one
sperms that
undergoes
duplication
“Diandric
diploidy”
10%
Tetraploid
fertilization of
a normal
ovum by
three sperms
“Dispermic
triploidy”
Karyotype
46XX
69XXX
69YXX
69YYX
46XX
46XY
Complete Partial
17. Familial biparental hydatidiform
mole
⚫Familial biparental hydatidiform mole (FBHM) is
inherited in an autosomal recessive pattern .
⚫Extensive mapping studies had demonstrated a
defective locus at 19q13.4. thisabnormality have been
localised toa singlegene- NALP7.
⚫This is the first causativegenedefect identified in H.
MOLE.
19. Feature
Karyotype
Partial mole
Most commonly
69, XXX or - XXY
Complete mole
Most commonly
46, XX or -,XY
Often present
Usually present
Variable, focal
Focal, slight-moderate
Absent
Absent
Diffuse
Diffuse, slight-severe
Pathology
Fetus
Amnion, fetal RBC
Villous edema
Trophoblastic proliferation
Clinical presentation
Diagnosis
Uterine size
Theca lutein cysts
Medical complications
Postmolar GTN
Missed abortion
Small for dates
Rare
Rare
1-5%
Molar gestation
50% large for dates
25-30%
10-25%
15-20%
Disaia &Creasman Clinical Gynecological Oncology 2007
Cunningham et al Williams Obsterics 23rd , 2010
20. What is the pathological features of
complete hydatidiform mole?
21. Complete H. Mole
Macroscopically, these microscopic changes transform the
chorionic villi into clusters of vesicles with variable
dimensions “ like bunch of grapes“.
No fetal or embryonic tissue are produced
Uterine enlargement in excess of gestational age .
Theca-lutein cyst associated in 30%
Microscopically Enlarged, edematous villi and abnormal
trophoblastic proliferation that diffusely involve the
entire villi.
No fetal tissue, RBCs or amnion are produced
23. Complete hydatidiform mole: Macroscopically, these
microscopic changes transform the chorionic villi into clusters of
vesicles with variable dimensions the name hydatidiform mole
stems from this "bunch of grapes"
25. CLINICAL FEATURES OF COMPLETE
MOLE
Historyof amenorrhoeaof 8-12 weeks
Irregular Vaginal bleeding- commonest (90%).
mayvary from spotting to profuse haemorrhage.
Expulsion of grapes likevesicles per vaginum (50%)
Lowerabdominal pain- a) overstretching of uterus
b) concealed haemorrhage
c) uterinecontraction toexpel out the content
d) infection
e) perforationof the uterus by invasive mole.
26. Hydatidiform Mole
Usually, in
association
with,
Theca lutein cysts (25-50%)
Very early onset Preeclampsia
( 26%)
Markedly elevated hCG 100,000
mIU/mL
Breathlessnessoracute respiratory
distress(2%)
Hyperemesis gravidarum (25%)
Hyperthyroidism (1-7%)
Excessive uterine enlargement
(50%)
27. Points to be noted during
examination
GENERAL EXAMINATION:
⚫Patient looks more ill and Pallor isoutof proportionof
bleeding.
⚫PR-tachycardia, RR- tachypnea /dyspnoea
⚫Features of preeclampsia present .usually there is early
onset of preeclampsia.
P/A-
⚫Uterine enlargement> than expected GA.
⚫The uterus is soft and doughydue toabsence of the
amniotic fluid sac.
⚫Fetal parts not felt
⚫FHS cannot be detected.
28. P/S-
⚫Cervical os may beopen orclose.
⚫Vuval orvaginal metastasis mayappearas purple
nodule.
P/V-
⚫Note the uterinesize.
⚫Internal ballotmentcannot beelicited.
⚫Unilateral or bilateral theca luteincystof ovary
palpable in 25-35% of cases.
30. Partial H. Mole
Microscopically: The enlarged, edematous villi and
abnormal trophoblastic proliferation are slight and
focal and did not involve the entire villi.
There is a scalloping of chorionic villi with undulating
border.
Fetal or embryonic or fetal RBCs
Macroscopically: The molar pattern did not involve
the entire placenta.
Uterine enlargement in excess of gestational age is
uncommon.
Theca-lutein cysts are rare
Fetal or embryonic tissue or amnion
31. Scalloping of chorionic villi
Partial Hydatidiform Mole
Trophoblastic proliferation are slight and focal
35. CLINICAL FEATURES OF PARTIAL
MOLE
History:
⚫Vaginal bleeding
⚫Usuallydiagnosed as missed or incomplete
abortion(91%).
Physical :
⚫A uteruscorrespondsorsmall forgestation age
⚫Excessiveuterinesize noted(4%)
⚫Toxemiaof pregnancy(4%)
36. Diagnosis:
History
Clinical examination
Ultrasound examination
Serum hCG levels
Histopathological examination
Cytogenetic and molecular biological examination
Immunostaining of p57kip2 gene recent
development in diagnosticaccuracy.it is a paternally
imprinted genewhich is maternallyexpressed
.positive in PHM
37. U/S is helpful in making a pre-evacuation diagnosis
but the definitive diagnosis is made by histological
examination.
U/S: Earlydetection reduced from 16 weeks (passageof
vesicles) to 12 wks
βhCG levels > 2 multiplesof the median may beof
value in thediagnosisoften exceeding 105 IU/l.
RCOG Guideline No. 38 ; 2010
38. Guideline to hCG Levels During Pregnancy
hCG levels in weeks from LMP (gestational age)* :
3 weeks LMP: 5 – 50 mIU/ml
4 weeks LMP: 5 – 426 mIU/ml
5 weeks LMP: 18 – 7,340 mIU/ml
6 weeks LMP: 1,080 – 56,500 mIU/ml
7 – 8 weeks LMP: 7, 650 – 229,000 mIU/ml
9 – 12 weeks LMP: 25,700 – 288,000 mIU/ml
13 – 16 weeks LMP: 13,300 – 254,000 mIU/ml
17 – 24 weeks LMP: 4,060 – 165,400 mIU/ml
25 – 40 weeks LMP: 3,640 – 117,000 mIU/ml
Non-pregnant females: <5.0 mIU/ml
Postmenopausal females: <9.5 mIU/ml
* These numbers are just a GUIDELINE– every woman’s level of
hCG can rise differently. It is not necessarily the level that
matters but rather the change in the level.
40. Complete hydatidiform mole. The classic "snowstorm"
appearance is created by the multiple placental vesicles.
41. In most patients with a partial mole,
the clinical and U/S diagnosis is
Usually missed or incompleteabortion.
Thisemphasizes the need fora
thorough histopathologicevaluationof
all missed or incompleteabortions
How Is Partial H .Mole Diagnosed?
RCOG Guideline No. 38 ; 2010
42. Classically: A thickened, hydropicplacentawith
fetal orembryonic tissue
Multiplesoft markers, including:
Cysticspaces in the placentaand
Transverseto AP dimension a ratio of the
gestationsacof > 1.5, is required forthe reliable
diagnosisof a partial molarpregnancy βhCG ≥
105 U/L
RCOG Guideline No. 38 ; 2010
How Is Partial H .Mole Diagnosed?
45. There are 2 important basic lines :
1 Evacuationof the mole
2Regular follow-up to detect
persistent trophoblasticdisease
If both basic lines are done
appropriately, mortalityratescan be
reduced to zero.
What Is The Plan of Management?
48. Management:
The patientshould be stabilized hemodynamically
Medical care:
Correction of:
i.
ii.
iii.
Anemia
Dehydration
Hyperthyroidism
iv. Hypertension
Surgical care
49. ⚫Suction Evacuation is method of choice –
can be done by conventional suction
curretageaswell as by MVA
⚫Two MVA setshould beavailable
⚫Cervical preparation with prostaglandinsor
misoprostol , should be avoided to reduce
the risk of embolisation
RCOG Guideline No. 38 ; 2010
What Is The Best Method Of
Evacuating A Molar Pregnancy?
50. For Partial mole: Itdepends on the fetal parts
Small fetal parts :Suction curettage
Large fetal parts: Medical (oxytocics)
In partial mole the oxytocics is safe ,as the hazard to
embolise and disseminate trophoblastic tissue is
very low
Also, the needing forchemotherapy is 0.1- 0.5%.
RCOG Guideline No. 38 ; 2010
Is That The Same For Partial Mole?
51. Canula up to a maximum of 12 mm, is usually
sufficient to evacuate all complete molar
pregnancies
52. Suction curettage has been performed
using 10mm canula under U/S guidance :
E
El
l SH
SHE
ER
RBIN
BINY
Y
H
O
S
H
O
S
P
P
Canula
53. Garner UpToDate 2010
Suction Curettage
⚫Supervision of seniorsurgeon
⚫Blood should becross matched and
keptavailable
⚫Maintain two i/v line
⚫Procedure to be carried out in OT
⚫Cervical os to bedilated up to 12mm
sizesuction cannula.
⚫Deep insertion of suction cannula
avoided
⚫Gentle curettage is performed after
evacuation is complete and tissue
sent for histopathology.
⚫ Intraop USG , if available help to
ensure thecomplitionof procedure.
• The useof oxytocin infusion priorto
completion of evacuation is not
recommended
55. When Anti-D Is Required?
It is required in Partial due to the presenceof
fetal RBCs
⚫In Complete mole because of poor
vascularisation of thechorionicvilli and
absence of the anti-D antigen, anti-D
prophylaxis is not required.
⚫Although ACOG recommend togive Anti-D
in all cases.
RCOG Guideline No. 38 ; 2010
56. Barrier methods – most preffered method.
Oral contraceptive method-Once βhCG level have
normalized: COC pill may be used.( as it mayactsas
growth factorfortrophoblastic tissue)
Lowdose OCP is preffered.
If oral COCwasstarted before thediagnosisof GTD
,COCcan becontinueas its potential to increase
risk of GTN isvery low
IUCD should not be used until β hCG levelsare
normal to reduceuterineperforation.
Permanentsterilisation- prefered in thosecouples
whose family has been completed.
What Is Safe Contraception Following GTD?
RCOG Guideline No. 38 ; 2010
57. Hysterectomy may be preferred to suction
curettage at age ≥ 40 years with no desire for
further pregnancies especially with other risk
factors for GTN as :
Large theca lutein cysts( >6 cm)
Significant uterine enlargement
Pretreatment βhCG ≥ 105 U/L.
Although hysterectomy does not eliminate
possibility of GTN, it markedly reduces its
likelihood. Post hyst. GTN is observed in 3-5%
of cases.
Soper. Obstet Gynecol 108:176, 2006 Garner UpToDate 2010
Cunningham et al,Williams Obstetrics,23rd ,2010
59. Second Uterine Evacuation : not required
routinely RCOG Guideline No. 38 ; 2010
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 *
It may be useful in the high-risk cases when
follow-up are unavailable or unreliable. * *
American College of Obstetricians and Gynecologists, 2004*
60. Prophylactic chemotherapy after
molar pregnancy
⚫The controversial practice of prophylactic
chemotherapy in GTN in women with H.mole is not
recommended ( According to recent cochrane data
based review 2012).
⚫ Overall PC reduces the risk of GTN however
researcherconsider thisevidence to be lowquality.
⚫When GTN did occurthe time todiagnosed in women
received PC is longer and these women require more
coursesare require tocure GTN.
⚫Unnecessary exposure to toxicadverseeffect.
61. ⚫Prophylactic Chemotherapy:
⚫In one randomized clinical trial, a single course of
methotrexate(0.4mg/ kg/day ) and folinicacid reduced
the incidence of postmolar trophoblastic disease from
47.4% to 14.3% in patients with high-risk moles:
Age >40 yrs
previous history of molar pregnancy
βhCG levels greater than 100,000 mIU/mL,
Uterine size greater than gestational age,
Ovarian sizegreater than 6 cm
All associated factors like PE, hyperthyroidism,
hyperemesis. Acute respiratorydistress.
Post evacuation uterine haemorrhage/subinvolution
⚫Still thegold standard is careful follow up
of each and every patient and serial
estimation of β HCG.
63. A baseline serum β -hCG level is obtained within 48
hoursafterevacuation.
Levelsare monitored everyweek till a normal value is
achieved. Level usually becomes normal by 8-10
weeks.
Monitor HCG every month forfurther 6 months from
the date of evacuation if HCG has to return to normal
within 56 daysafterpregnancyevent.
>56 daysof the pregnancyevent :Follow up is 6 months
from normalization of the hCG level.
These levelsshould progressively fall toan undetectable
level (<5 mu/ml).
RCOG Guideline No. 38 ; 2010
The Post-evacuation Surveillance. How?
64. In resource poor setting – UPT and USG.
Monthly USG 1 month after evacuation.
UPT should be perfomed once monthly starting from 3rd to
4th month untill 1 year after evacuation.
The normal time for βhCG to normalise is 99 days in
complete moles and 59 days in partial mole.
Pelvic examination:
⚫ Duration: while hCG is elevated to monitor the
involution of pelvic structures and to aid in the
identification of vaginal metastasis
65. Hydatidiform Mole
⚫Complications associated with molar pregnacy:
⚫ Theca-luteincysts
⚫ Pre eclampsia,
⚫ hyperthyroidism,
⚫ Respiratorydistress
⚫ Hyperemesis
⚫ Uterineperforation ,
⚫ Excessive haemorrhage,
⚫ Respiratory distress syndrome.
⚫ Development of persistent mole.
66. Theca lutein cyst (>5-6cm)
(25-35%)
pain or
pressure
torsion, ruptureor
bleeding
post molar
GTD
Requireaspiration require
opherectomy
The mean time fortheca luteal cysts toregress isapproximately 8 weeks
67. RESPIRATORY DISTRESS SYNDROME
(rare event)
Pathophysiology:
⚫embolisation of trophoblastic tissue , pulmonary
metastasis
⚫ Risk factors :
⚫uterinesize > 14-16 weeks
⚫ high HCG level
⚫Contributing factors- anaemia, thyrotoxicosis
It should resolvewithin 24 to 48 hoursafter molarevacuation
68. Hyperthyroidism:
⚫Prevalence:
⚫ Clinical hyperthyroidism is seen in less than 10% of
patientswith molarpregnancies
⚫ Management:
⚫ Beta-blockers should be administered prior to
molarevacuation to prevent thyroid storm that
may be induced byanesthesiaand surgery.
69. When can women whose last pregnancy was a
complete or partial hydatidiform molar
pregnancy try to conceive in the future ?
⚫Womenshould beadvised not toconceiveuntil
their follow-up is complete.
⚫Womenwho undergochemotherapyareadvised
not toconceive for 1 yearaftercompletionof
treatment.
⚫Patientwith metastatic GTN – 2 years
70. Pregnancy after Hydatidiform Mole:
⚫Risk of another molarpregnancy:
(1–2% incidence)
⚫Current recommendations for
managementof subsequent pregnancies:
⚫P/V in first trimesterand ultrasound toconfirm
normal gestational developmentand dates
⚫Examination of the placentaorproductsof
conception histologicallyat the timeof delivery
orevacuation .
⚫An hCG level should be obtained 6 weeks
and 10 weeks post evacuation or delivery
to confirm normalization.
71. A hydatidiform mole and a co-existent
fetus:
⚫Prevalence: Rare (0.005%-0.01% pregnancies)
⚫ Diagnosis:
⚫ Ultrasound
⚫ In diagnosticdoubt , invasive testing for karyotyping to
be done.
⚫ Examinationof the placenta following delivery.
Outcome of such pregnancies is poor live birth of 25%,
increased risk of early fetal loss(40%), preterm
labour(36%) ,pre eclampsia.
⚫Complications: Increased risk of medical complications
⚫ Increased risk forpostmolargestational trophoblastic
disease.
72. False-positive hCG values, also known
as “phantom hCG”
Cause: the presence of non-specific
heterophil antibodies in the patients’ sera.
⚫Should be suspected if hCG values plateau
at relatively low levels and do not respond
to therapeutic maneuvers
⚫Evaluation of patients with :
• Urinary hCG
• Serial dilutionsof the serum
73. Prognosis:
⚫Post-molar gestational trophoblastic disease:
⚫ Risk:
⚫ Following complete mole: 20%
⚫ Following partial mole: 5%
⚫ Type:
⚫ 70% to 90% are persistentor invasive moles
⚫ 10% to 30% are choriocarcinomas.
Recurrence-
Risk of recurrencwith prior molar pregnancy is
1-4%
74. PERSISTENT GESTATIONAL TROPHOBLASTIC
DISEASE
⚫It is defined as persistence of trophoblastic activity as
evidnced by clinical ,imaging, pathological and
hormonal study following initial treatment.
⚫It may be followingtreatment of hydatiform mole,
invasive mole, choriocarcinoma or placental site
trophoblastic tumour.
INVASIVE MOLE-
In which the trophoblastic tissue invade the
myometrium.
75. Criteria for diagnosis of gestational
trophoblastic neoplasia or post molar GTD
⚫ Plateau of serum β-hcg level (+/-10%) forfour measurements
during a period of 3 weeksor longer– days 1,7,14,21.
⚫ Riseof serum β-hcg > 10% during threeweeklyconsecutive
measurementor longer, during a period of 2 weeksor more –
days 1,7,14.
⚫ The serum β -hcg level remainsdetectable for 6 monthsor more
after moleevacuation.
⚫ Histological criteria forchoriocarcinoma.
77. Staging
International staging of WHO may be summarized as
follows:
Ⅰ : lesion localized in uterus, no metastasis;
Ⅱ: lesion extends beyond uterus, but still confined to
internal genitalias;
Ⅲ
: pulmonary lesion
Ⅳ: metastasis tootherdistantsites.
78. Indication for therapy
Indication for therapyafterevacuation-
⚫An abnormal hcg regression pattern (10% or> rise in hcg
level or plateauing hcg or 3 stablesvalueover 2 weeks)
⚫An hcg rebound.
⚫Histological diagnosis of choriocarcinoma or placental site
trophoblastic tumour.
⚫The presenceof metastases.
⚫High hcg levels(.20,000miu/ml more than 4 weeks
postevacuation)
⚫Persistentlyelevated hcg levels 6 months post evacuation.
79. Hydatiform mole
Evacuation
Serial hcg level resolution
GTN
FIGO scoring
Low risk(≤6) high risk(>6)
Single agent (MTX)
chemotherapy
combination(MAC/EMACO)
chemotherapy
Serial hcg level resolution(life–long
follow up)
Relapse /resistantdisease
Second –linechemotherapy ±surgical debulking