1. Thyroid disorders are common in pregnancy, affecting 1-2% of pregnant women. Optimal management is important for pregnancy outcomes.
2. Hypothyroidism and hyperthyroidism can cause complications for both mother and fetus if not treated properly. Levothyroxine is the treatment of choice for hypothyroidism. Antithyroid drugs are used to treat hyperthyroidism.
3. Factors like hCG and estrogen increase thyroid function in pregnancy, requiring adjustments to diagnosis and treatment of thyroid disorders compared to non-pregnant individuals. Monitoring of thyroid levels is important during and after pregnancy.
Thyroid disorders are common in pregnancy . This is potential treatable cause of bad obstetric history .Hypothyroidism and hyperthyroidism both should be screened for clinically as well as by laboratory tests .
Due to availability of Thyroid testing ,it is more easily diagnosed and Treated.
Hypothyroid mother if not adequately treated ,there is poor mental development of the baby.
Due to awareness more and more diagnosis is made .There should be universal screening for thyroidal illness in pregnancy .
Over the past several years it has been proved that maternal thyroid disorder influence the outcome of mother and fetus, during and also after pregnancy. The most frequent thyroid disorder in pregnancy is maternal hypothyroidism. It is associated with fetal loss, placental abruptions, pre-eclampsia, preterm delivery and reduced intellectual function in the offspring.1 In pregnancy, overt hypothyroidism is seen in 0.2% cases2 and sub clinical hypothyroidism in 2.3% cases3. Fetal loss, fetal growth restriction, pre-eclampsia and preterm delivery are the usual complications of overt hyperthyroidism (low TSH and high T3, T4) seen in 2 of 1000 pregnancies whereas mild or sub clinical hyperthyroidism (suppressed TSH alone) is seen in
1.7% of pregnancies and not associated with adverse outcomes4. Autoimmune positive euthyroid pregnancy shows doubling of incidence of miscarriage and preterm delivery. Worldwide more than 20 million people develop neurological sequel due to intra uterine, iodine deprivation5. Other problems of thyroid disorders in pregnancy are post partum thyroiditis, thyroid nodules and cancer, hyper emesis gravidarum etc. Debates and disputes persist regarding several protocol and management plan in this specific spectrum of diseases.
A normal pregnancy results in a number of important reversible physiological and hormonal changes that alter thyroid structure and more importantly function.
Understanding these change are important to interpreting, identifying and managing of thyroid disease in pregnancy.
Thyroid disease in_pregnancy
Presented by: Dr. Ahmad mukhtar
M.B.B.Ch., M.Sc Obstetrics and GynecologyAssistante lecturer of Obstetrics and Gynecology
Faculty of Medicine, Zagazig University
Thyroid disorders are common in pregnancy . This is potential treatable cause of bad obstetric history .Hypothyroidism and hyperthyroidism both should be screened for clinically as well as by laboratory tests .
Due to availability of Thyroid testing ,it is more easily diagnosed and Treated.
Hypothyroid mother if not adequately treated ,there is poor mental development of the baby.
Due to awareness more and more diagnosis is made .There should be universal screening for thyroidal illness in pregnancy .
Over the past several years it has been proved that maternal thyroid disorder influence the outcome of mother and fetus, during and also after pregnancy. The most frequent thyroid disorder in pregnancy is maternal hypothyroidism. It is associated with fetal loss, placental abruptions, pre-eclampsia, preterm delivery and reduced intellectual function in the offspring.1 In pregnancy, overt hypothyroidism is seen in 0.2% cases2 and sub clinical hypothyroidism in 2.3% cases3. Fetal loss, fetal growth restriction, pre-eclampsia and preterm delivery are the usual complications of overt hyperthyroidism (low TSH and high T3, T4) seen in 2 of 1000 pregnancies whereas mild or sub clinical hyperthyroidism (suppressed TSH alone) is seen in
1.7% of pregnancies and not associated with adverse outcomes4. Autoimmune positive euthyroid pregnancy shows doubling of incidence of miscarriage and preterm delivery. Worldwide more than 20 million people develop neurological sequel due to intra uterine, iodine deprivation5. Other problems of thyroid disorders in pregnancy are post partum thyroiditis, thyroid nodules and cancer, hyper emesis gravidarum etc. Debates and disputes persist regarding several protocol and management plan in this specific spectrum of diseases.
A normal pregnancy results in a number of important reversible physiological and hormonal changes that alter thyroid structure and more importantly function.
Understanding these change are important to interpreting, identifying and managing of thyroid disease in pregnancy.
Thyroid disease in_pregnancy
Presented by: Dr. Ahmad mukhtar
M.B.B.Ch., M.Sc Obstetrics and GynecologyAssistante lecturer of Obstetrics and Gynecology
Faculty of Medicine, Zagazig University
hyperthyroidism, thyrotoxicosis, grave disease, thyroid storm, pregnancy, high risk pregnancy, pregnancy complications, management of thyrotoxicosis and thyroid storm in pregnancy
Due to pregnancy thyroid economy is affected with changes in iodine metabolism, TBG and development of maternal goiter. The incidence of hypothyroidism in pregnancy is quite common with autoimmune hypothyroidism being the most important cause. Overt as well as subclinical hypothyroidism has a varied impact on maternal and neonatal outcome. After multiple studies also, routine screening in pregnancy for hypothyroidism can still not be recommended. Management mainly comprises of dosage adjustments as soon as pregnancy is diagnosed based on results of thyroid function tests. The aim should be to keep FT4 at the upper end of normal range.
Hypothyroidism in pregnancy by DR ALKA MUKHERJEE DR APURVA MUKHERJEE NAGPUR M.S.alka mukherjee
Pregnancy is a period that places great physiological stress on both the mother and the fetus. When pregnancy is compounded by endocrine disorders such as hypothyroidism, the potential for maternal and fetal adverse outcomes can be immense. While a lot of attention has been focused on the adverse fetal outcomes consequent to hypothyroidism, attention is also being gradually directed towards the adverse maternal outcomes of this disorder. Role of antibody positivity in influencing outcomes in a euthyroid woman, also needs further clarification. Prompt diagnosis and treatment of hypothyroidism in pregnancy is very essential. Subclinical hypothyroidism also needs to be detected and treated to prevent adverse outcomes, especially maternal. Since women with hypothyroidism during pregnancy, especially of the autoimmune variety might have a flare up of the disorder post-partum, or might continue to require thyroxine replacement post-partum, adequate follow-up is mandatory. While targeted case finding is generally practised, recent evidence seems to indicate that universal screening might be a better option. In conclusion, routine screening, early confirmation of diagnosis and prompt treatment. Allied with regular post-partum follow up, is required to ensure favourable maternal and fetal outcomes.
Thyroid physiology is perceptibly modified during normal pregnancy. These alterations take place throughout gestation, help to prepare the maternal thyroid gland to cope with the metabolic demands of pregnancy, are reversible post-partum and the interpretation of these changes can pose a challenge to the treating physician.
Hypothyroid Disorders in Obs & Gynae – Case based approach – Part -1 Lifecare Centre
Hypothyroid Disorders in Obs & Gynae – Case based approach – Part -1
Moderator - Dr Meenakshi Sharma
& Dr Puja Dewan
Panelist
Dr Dipti Nabh
Dr Richa Singhal
Dr Manju Sharma
Dr Deepa Gupta
Dr Renu Chawla
Dr Anita Agarwal
hyperthyroidism, thyrotoxicosis, grave disease, thyroid storm, pregnancy, high risk pregnancy, pregnancy complications, management of thyrotoxicosis and thyroid storm in pregnancy
Due to pregnancy thyroid economy is affected with changes in iodine metabolism, TBG and development of maternal goiter. The incidence of hypothyroidism in pregnancy is quite common with autoimmune hypothyroidism being the most important cause. Overt as well as subclinical hypothyroidism has a varied impact on maternal and neonatal outcome. After multiple studies also, routine screening in pregnancy for hypothyroidism can still not be recommended. Management mainly comprises of dosage adjustments as soon as pregnancy is diagnosed based on results of thyroid function tests. The aim should be to keep FT4 at the upper end of normal range.
Hypothyroidism in pregnancy by DR ALKA MUKHERJEE DR APURVA MUKHERJEE NAGPUR M.S.alka mukherjee
Pregnancy is a period that places great physiological stress on both the mother and the fetus. When pregnancy is compounded by endocrine disorders such as hypothyroidism, the potential for maternal and fetal adverse outcomes can be immense. While a lot of attention has been focused on the adverse fetal outcomes consequent to hypothyroidism, attention is also being gradually directed towards the adverse maternal outcomes of this disorder. Role of antibody positivity in influencing outcomes in a euthyroid woman, also needs further clarification. Prompt diagnosis and treatment of hypothyroidism in pregnancy is very essential. Subclinical hypothyroidism also needs to be detected and treated to prevent adverse outcomes, especially maternal. Since women with hypothyroidism during pregnancy, especially of the autoimmune variety might have a flare up of the disorder post-partum, or might continue to require thyroxine replacement post-partum, adequate follow-up is mandatory. While targeted case finding is generally practised, recent evidence seems to indicate that universal screening might be a better option. In conclusion, routine screening, early confirmation of diagnosis and prompt treatment. Allied with regular post-partum follow up, is required to ensure favourable maternal and fetal outcomes.
Thyroid physiology is perceptibly modified during normal pregnancy. These alterations take place throughout gestation, help to prepare the maternal thyroid gland to cope with the metabolic demands of pregnancy, are reversible post-partum and the interpretation of these changes can pose a challenge to the treating physician.
Hypothyroid Disorders in Obs & Gynae – Case based approach – Part -1 Lifecare Centre
Hypothyroid Disorders in Obs & Gynae – Case based approach – Part -1
Moderator - Dr Meenakshi Sharma
& Dr Puja Dewan
Panelist
Dr Dipti Nabh
Dr Richa Singhal
Dr Manju Sharma
Dr Deepa Gupta
Dr Renu Chawla
Dr Anita Agarwal
Thyroid Disorder:
Thyroid disease is the second most common endocrine disorder affecting women of reproductive age, and when untreated during pregnancy is associated with an increased risk of miscarriage, placental abruption, hypertensive disorders, and growth restriction.
Types of thyroid disorder incidence in pregnancy:
1. Hypothyroidism 0.05%
2. Hyperthyroidism 0.05-0.2%
3. Postpartum thyroiditis 5-10%
Signs:
Hair loss
Sweating
Irritability
Bulging eyes
Rapid heart beat
Nervousness
Tremor of fingers
Difficulty sleeping
Weight loss
Thyroid Disorders in Obs & Gynae - Case based approach onHyperthyroidism & T...Lifecare Centre
Thyroid Disorders in Obs & Gynae - Case based approach onHyperthyroidism & Thyroid Cancer--- Part 2
Moderator - Dr Meenakshi Sharma
& Dr Puja Dewan
Panelist
Dr Dipti Nabh
Dr Richa Singhal
Dr Manju Sharma
Dr Deepa Gupta
Dr Renu Chawla
Dr Anita Agarwal
Hypothyroidism is a condition marked by an underactive thyroid gland and may be present during pregnancy. It incidence
0.05% of pregnant women
31% positive for TPO Ab
Associated with Gest Hypertension.
Hyperthyroidism in pregnancy:
Hyperthyroidism is characterized by high level of serum thyroxine and triiodothyronine, low levels of thyroid-stimulating hormones.
Hyperthyroidism during pregnancy usually is caused by an
Autoimmune disorder called Grave’s disease. It incidence :-
- 0.2% of pregnant women
- 95% Grave’s disease
It is a presentation on Thyroid Disorder in Pregnancy 2023
Detailed presentation on congenital hypothyroidism including physiology, pathophysiology, newborn screening, management and follow up (including Sri Lankan practice).
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Basavarajeeyam - Ayurvedic heritage book of Andhra pradesh
Thyroid disorders in pregnancy
1. THYROID DISORDERS IN
PREGNANCY
-Dr. Karthik(Final yr PG)
Dr.Spandana(First yr PG)
Moderators-
Dr.P.L.John Israel(HOD)
Dr.Nagarjuna Reddy(Asst.prof)
2. • Most common endocrine disorder in pregnancy.
• 1-2% pregnant women.
• Pregnancy may modify course of thyroid
disease.
• Pregnancy outcome can depend on optimal
management of thyroid disorders.
3.
4.
5.
6. PREGNANCY AND THE THYROID
• Human Chorionic Gonadotropin - a
glycoprotein heterodimer - α-subunit
(identical to that of TSH, LH, and FSH) and a
specific β-subunit, which has similarity to TSH.
• binds and stimulates the Human TSH Receptor
• 1 U hCG = 0.7 μU of human TSH
• In high concentrations hCG will cause
hyperthyroidism characterized by a diffuse
goiter, elevated free T4, and suppressed TSH.
7. FIVE FACTORS THAT ALTER THYROID
FUNCTION IN PREGNANCY:
1. The transient increase in hCG during the first trimester, which
stimulates the TSH-R.
2. The estrogen-induced rise in TBG during the first trimester, which
is sustained during pregnancy.
3. Alterations in the immune system, leading to the onset,
exacerbation, or amelioration of an underlying autoimmune
thyroid disease.
4. Increased thyroid hormone metabolism by the placenta.
5. Increased urinary iodide excretion, which can cause impaired
thyroid hormone production in areas of marginal iodine
sufficiency.
13. DIAGNOSIS
NORMAL RANGE OF TSH IN EACH TRIMESTER
• First trimester – 0.1-2.5 mIU/L
• Second trimester – 0.2-3.0 mIU/L
• Third trimester – 0.3-3.0 mIU/L
14. • Overt hypothyroidism – TSH 2.5-10
Low FT4 (or)
TSH≥ 10 mIU/ L
• Subclinical hypothyroidism – 2.5-10 &
Normal FT4
• Isolated hypothyroxinemia – Normal TSH &
Low F T4
15. TSH MONITORING
• During pregnancy –
Every 4 weeks until 16-20 weeks gestation.
At once between 26-32 weeks gestation
• After delivery –
Stop or titrate down levothyroxine .
Decrease dose by 30%(diagnosed in pregnancy)
Prepregnancy dose(hypothyroid before pregn.)
Retest TSH levels in 4-8 weeks
16. SHOULD EVERY ANTENATAL PT. BE SCREENED
DURING FIRST TRIMESTER?
• Acc. to ATS, “universal FT4 screening of pregnant
women is not recommended”
• The Endocrine Society does not recommend universal
screening, but encourages TSH measurement of
‘high-risk‘ individuals, and also promotes prenatal
low-dose L-thyroxine (T4) therapy, with a target TSH of
less than 2.5 mIU/l.
• The ITS guidelines clearly recommend that “all
pregnant women should be screened at 1st antenatal
visit by measuring TSH levels”, and highlight that
“ideally screening should be carried out during
pre-pregnancy evaluation or as soon as pregnancy is
confirmed”
17. Should every patient with a normal TSH during
first trimester be screened again during
subsequent trimesters?
• ATA/TES/ITS suggests regular TSH monitoring
for euthyroid antibody positive woman
throughout gestation.
19. SHOULD EVERY ANTENATAL Pt. WITH SUBCLINICAL
HYPOTHYROIDISM ( TSH>2.5 mIU/L) BE TREATED?
• For a TSH value >10.0 mIU/l, L-thyroxine
supplementation is mandatory. For those with
a TSH <2.5 mIU/l during first trimester, no
further investigations are needed.
• A FT4 estimation is indicated for patients with
a TSH of 2.5-10 mIU/l.
• A normal FT4 should ideally elicit a thyroid
antibody test, with therapy being initiated in
all antibody-positive patients.
20. • Treat all patients with overt hypothyroidism
(TSH > 10 mIU/l; TSH > 2.5 mIU/l with low
FT4); and all subclinically hypothyroid patients
with antibody positivity (TSH > 2.5 mIU/l,
TAb+)
• Isolated hypothyroxinemia-Need not be
treated
21. OPTIMAL TREATMENT OF OH/SCH
• Oral LT4 (1.6 μg/Kg)
• Other thyroid preparations such as T3 not to
be used
• Levothyroxine sodium – most widely
prescribed
• Safe for both mother and fetus (Category A)
• Available dosages – 12.5 – 300 μg
22. • If alreadly hypothyroid – 30 % increase from
non-pregnant value
• If newly diagnosed in pregnancy: 1-2 μg/kg/d
approx. 100-150μ of levothyroxine daily
23. WOMEN NOT ON LEVOTHYROXINE BEFORE
PREGNANCY-Start if TSH> 2.5 in I trimester
(esp if TPO Ab+)
THYROTROPIN(TSH)
LEVELS DURING FIRST
TRIMESTER
STARTING DOSE OF
LEVOTHYROXINE
2.5-5.0 mIU/L 50 μg / day
5.0-8.0 mIU/L 75 μg / day
> 8.0 mIU/L 100 μg / day
24. CLINICAL GUIDELINES FOR IODINE
NUTRITION
• Because of increased thyroid hormone
production, increased renal iodine excretion, and
fetal iodine requirements, dietary iodine
requirements are higher in pregnancy than they
are for nonpregnant adults.
• Normal levels of thyroid hormone are essential for
neuronal migration and myelination of the fetal
brain.
• Iodine deficiency is the leading cause of
preventable mental retardation worldwide.
25. • Spot urinary iodine values are used most
frequently for determination of iodine status in
general populations.
• Whose median urinary iodine concentrations are
50–150 mg/L are defined as mildly to moderately
iodine deficient.
• WHO recommends 250 µg/d for pregnant women
and for lactating women.
• Dietary Iodine sources-Iodised salt
Sea food
Eggs, meat
26. WHAT IS THE SAFE UPPER LIMIT FOR IODINE
CONSUMPTION IN
PREGNANT AND BREASTFEEDING WOMEN?
• Wolff–Chaikoff effect – High iodide levels
inhibiting thyroid hormone release
• Sustained iodine intake from diet and dietary
supplements exceeding 500–1100 mg daily
should be avoided due to concerns about the
potential for fetal hypothyroidism.
27. TAKE HOME MESSAGE
1. ITS – Compulsory screening at first antenatal
visit
2. All patients with SCH and OH should be treated
3. DOC- LT4 – 1.6μg/kg
4. TSH monitoring during pregnancy – Every 4
weeks until 16-20 weeks gestation
5. After delivery – titrate the dose
6. Recommended iodine intake - 250 µg/d
30. THYROTOXICOSIS IN PREGNANCY
• Def-‘‘The clinical syndrome of hyper
metabolism and hyperactivity that results when
the serum concentrations of free thyroxine
hormone (T4) and/or free triiodothyronine (T3)
are high.’’
31. • Graves’ disease - most common cause of
autoimmune hyperthyroidism in pregnancy
( 0.1%–1%).
non-autoimmune causes
• toxic multinodular goiter,
• toxic adenoma,
• factitious thyrotoxicosis,
• Subacute painful or silent thyroiditis or
• Struma ovarii.
32. Transient Gestational Thyrotoxicosis
• A physiologic mild transient gestational
thyrotoxicosis (GTT) or hyperthyroidism - in
the late first trimester of normal pregnancy
• An exaggeration of this physiologic increase in
thyroid stimulation in the first trimester may
also be seen in some women and is associated
with high levels of hCG (100,000-200,000 U/L),
such as those found in twin pregnancies
33. • self-limited
• Risk of birth defects warrants against the use
of antithyroid drugs in early pregnancy
• in rare circumstances-low doses of PTU (100-
200 mg /day or less) may be required for a few
weeks until the hCG falls spontaneously.
• It may be difficult to separate this syndrome
from early Graves disease, and a TRAb test
may be helpful
34. Abnormal Responses to hCG
• A few patients have been reported with an
inherited variant of GTT in which a mutation
in the TSHR gene resulted in a receptor
protein with an increase in its responsiveness
to hCG
• Such patients develop hyperthyroidism even
with physiologic serum hCG concentrations.
35. GRAVES DISEASE DURING PREGNANCY AND THE
POSTPARTUM PERIOD
• Overactive thyroid - seen in 0.2% of pregnant
women
• Lower incidence of Graves disease is due to
suppression of autoimmune responses during
pregnancy
• Thyrotoxicosis has a variety of negative
influences on fertility itself & also associated
with increased pregnancy loss and serious
medical complications for both the mother
and the infant
36. THYROID ABs IN PREGNANT PATIENTS WITH
GRAVES DISEASE
• The hallmark of the immune effects initiated
by the placenta - fall in thyroid AutoAbs
—TPO-Ab, Tg-Ab, and TRAbs
• Secondary to enhanced regulatory T-cell
activity
• Followed by rapid increase in autoantibody
levels after the immunosuppression is lost in
the postpartum period
37. • Assays for TRAbs in the serum of pregnant
women with Graves disease may be of clinical
value in selected cases because a failure of this
immunosuppression may indicate potential fetal
problems.
• Because maternal Abs cross the placenta –
stimulate fetal thyroid causing thyrotoxicosis.
• High levels of TRAbs, usually greater than three
times the upper normal limit, are correlated with
fetal thyroid stimulation
38. PREGN. WOMEN AT RISK FOR FAILURE
TO SUPPRESS THYROID AUTOAbs
• include :
• those with more severe hyperthyroidism
• those with significant Grave’s Ophthalmopathy
• With infiltrative dermopathy.
• In addition, the prior treatment of the mother,
especially with radioiodine, may not always be accomp.
by a sufficient ↓ in TRAbs.
Thus, the fetus may still be at risk for development of
fetal or neonatal thyrotoxicosis,
So, the mother may need antithyroid drug treatment and
the fetus monitored by umbilical cord blood testing
and USG
39. Differential Diagnosis
• GTT secondary to hCG stimulation of the
thyroid gland
• When it is more severe it is usually due to
Graves disease because toxic MNGs and hot
nodules are uncommon in this age group
40.
41.
42. DIAGNOSIS
• Pregnancy & hyperthyroidism - both accomp. by
thyroid stimulation, a hyperdynamic circulation,
and hypermetabolism
• In pregnancy, S. TBG levels are increased
• Thus in both conditions, the total S. T4 and T3
levels are elevated so that the upper limit of
normal range during second and third trimesters
of gestation is about 1.5 times the nonpregnant
range
43. • Diagnosis of thyrotoxicosis is confirmed when
S. TSH level is below the trimester specific
lower limit and the total / free T4 levels above
the N range
• Detection of TRAbs can confirm the diagnosis
of Graves disease
44. COMPLICATIONS OF
HYPERTHYROIDISM IN PREGNANCY
• Increased and recurrent pregnancy loss
• Preterm delivery
• Preeclampsia
• Fetal growth restriction
• Fetal thyroid hyperfunction or hypofunction caused by
TRAbs
• Fetal goiter from excessive antithyroid drug treatment
• Neonatal thyrotoxicosis
• Increased perinatal and maternal mortality risk
• Potential for decreased IQ of offspring because of
excessive use of antithyroid drugs
45. TREATMENT
• Medical therapy is the method of choice in pregnancy.
• Because of the usual improvement in the disease, the
dosage of antithyroid drug req. to control the disease in the
later phases of pregnancy - less than nonpregnant dosage.
• Overtreatment of the hyperthyroid pregnant woman-
associated with potentially severe consequences for the
fetus.
• Thus, the clinician should prefer mild undertreatment to
avoid the risk of hypothyroidism
46. ANTITHYR. DRUGS
• PTU and methimazole readily and rapidly cross
the placenta equally well and are concentrated in
the fetal thyroid.
• In excess quantity these agents can cause
goitrous hypothyroidism in the fetus
• Transplacental passage of maternal TRAbs in the
latter half of pregnancy can result in fetal thyroid
stimulation.
• Therefore, the fetal thyroid is subject to the
same factors that influence maternal thyroid
hormone production
47. • Until recently, the antithyroid drug of choice
throughout pregnancy was PTU
• But because of the rare yet serious side effect of
PTU-induced hepatic failure , in June 2009 the
FDA issued an advisory that PTU should be
reserved for the first trimester of pregnancy
while organogenesis is occurring
• Subsequently, methimazole could be prescribed.
• Guidelines recommend the use of PTU in the first
trimester and to consider shifting from
methimazole to PTU in women planning a
pregnancy
48. DOSES OF Antithyroid Drugs
• PTU – 300-450mg/day given in 3 oral doses of
100-150mg each
• Carbimazole – 10-40 mg daily
• Methimazole – 5-30mg daily
• Therapeutic antithyroid potency ratio of
methimazole to PTU is around 20 : 1.
• Thus, a patient who requiring 50 mg of PTU in the
first trimester may be given 2.5 mg methimazole,
and she may not even require a thionamide
during the later part of pregnancy
50. • PTU is also teratogenic, and the use of PTU is also
associated with minor birth defects
• estimated to be around 1 in 40 exposed(Vs. 1 in
30)
• The associated defects include: preauricular
sinuses and cysts and urinary tract abnormalities
• The serum TSH concentration should be
monitored monthly—more to avoid inadvertent
overtreatment rather than as the target for
normalization
51. Iodide and Beta Blockers
• Therapeutic radioiodine is Contraindicated in pregnancy
• Iodide itself should also not be used as therapy for more
than 2 to 3 wks - crosses the placenta - induce a large goiter
that may cause airway obstruction in the newborn.
• Propranolol or other beta blockers can cause IUGR, delayed
lung development, and neonatal hypoglycemia /
depression
52. Surgery
• Not desirable - during the first and third trimesters –
‘coz of induction of early pregnancy loss / premature
labor
• Iodide for 7 -10 days to ↓ size and vascularity
• TRAb will not disappear immediately after Sx
• Thus, the fetal thyroid may still be stimulated, and
withdrawal of antithyroid drugs from the pregnant
woman may lead to isolated fetal hyperthyroidism
53. • Indications: severe refractory hyperthyroidism,
intolerance of medications,
agranulocytosis,
noncompliance or
malignancy.
• Ideally surgery is delayed until postpartum.
• During pregnancy : best accomplished in the
second trimester.
54. GRAVES DISEASE IN THE POSTPARTUM
PERIOD
• Following delivery, the immune changes are
slowly lost and a return to normal
• 4 to 12 months post partum— New-onset or
recurrent thyrotoxicosis is seen. Such thyroid
dysfunction may be transient or permanent.
55. Transient postpartum thyroiditis
• most common form of postpartum hyperthyr.
-precedes a period of hypothyroidism
• due to thyroid cell destruction and may occur
in approx. 5-10% of patients
56. POSTPARTUM THYROTOXICOSIS
• The patients with Graves disease and postpartum
thyrotoxicosis were classified into three categories:
1. Persistent recurrent hyperthyroidism with an
elevated Radio Active Iodine Uptake (classic Graves
disease).
2. A transient disorder a/w a normal or an ↑ RAIU
(transient Graves disease).
3. Some patients, esp. those with the highest titers of
TPO Abs, experienced the transient thyrotoxicosis
with a ↓RAIU (the thyrotoxic phase of postpartum
thyroiditis referred to earlier). This phase, inturn, may
be followed by a hypothyroid phase.
57.
58. Preconception Counseling
• If the patient wishes to conceive in the near future and is in
early remission after a course of antithyroid drug treatment ,
antithyroid drugs can be reluctantly reintroduced if required
during pregnancy if symptomatic thyrotoxicosis recurs.
• If the patient is being treated with antithyroid agents for
active Graves ds., definitive therapy (radioiodine therapy or
surgery) should be considered to forestall the complexities of
managing hyperthyroidism during pregnancy.
59. NURSING AND ANTITHYROID DRUGS
• Little difference b/w secretion of PTU and
methimazole in milk
• The drug doses transferred via breast milk are
very small, and no drug side effects have been
reported in neonates whose mothers were
taking antithyroid drugs, although periodic
tests of neonatal thyroid function may be
appropriate in women taking very high doses.
60. TAKE HOME MESSAGE
• Grave‘s ds vs. GTT – TRAbs
• PTU in first trimester
• PTU – 300-450mg/day given in 3 oral doses of
100-150mg each
• Carbimazole – 10-40 mg daily
• Methimazole – 5-30mg daily
• Monthly monitoring of TSH
• Surgery - 2nd trimester
61. REFERENCES
• William’s Textbook of Endocrinology, 13th Ed.
• ATA guidelines 2016-2017
• Indian Journal of Endocrinology And
Metabolism – 2013 (ITS guidelines)
• The Endocrine Society, 2012
Editor's Notes
H.Mole and chorio ca.--- high levels of hcg
0.4 to 4.2 mU/L- N TSH levels
The normal range
for free T4 is 9 to 30 pmol/L (0.7 to 2.5 ng/dL), and for free
T3 the range is 3 to 8 pmol/L (0.2 to 0.5 ng/dL
Localised/wide spread areas of missing skin-aplasia cutis
but large studies have suggested that it can be employed with safety for short periods or at very low doses.