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
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
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.
what is endometriosis? Theories in endometriosis, sites of endometriosis. types and clinical presentation. signs and symptoms.
Investigations :TVS, CA125
laparoscopic findings
chocolate cyst and extrapelvic endometriosis.
Classification of endometiosis
Diffential diagnosis
Management :of asymptomatic and symptomatic cases
drugs and minimally invasive surgery
surgey and preventive measures in endometiosis.
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.
what is endometriosis? Theories in endometriosis, sites of endometriosis. types and clinical presentation. signs and symptoms.
Investigations :TVS, CA125
laparoscopic findings
chocolate cyst and extrapelvic endometriosis.
Classification of endometiosis
Diffential diagnosis
Management :of asymptomatic and symptomatic cases
drugs and minimally invasive surgery
surgey and preventive measures in endometiosis.
Detailed presentation on congenital hypothyroidism including physiology, pathophysiology, newborn screening, management and follow up (including Sri Lankan practice).
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 .
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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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.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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12. IODINE DEFICIENCY GOITER
Leading cause of preventable Mental retardation
(developing countries)
Mean IQ loss 13.5points
Median Urinary Iodine Excretion determine iodine
sufficiency
Iodine requirement
Non pregnant 150μg
Pregnancy 175μg
Lactation 200μg
17. LYMPHOCYTIC HYPOPHYSITIS
Secondary hypothyroidism
Peripartum period
Autoimmune
Ant pituitary destruction
Panhypopituitarism to single hormone deficiency
Mass effects (headache & visual changes)
Imaging: enhancing sella turcica mass
18. SUBCLINICAL HYPOTHYROIDISM
TSH & Normal FT4 & FT3
2-5% in pregnancy
31% positive for TPO Ab
Associated with Gest HTN, preterm deliveries, stillbirths,
abruption.
Fetal psychomotor development may be impaired
Routine screening not recommended
19. ISOLATED HYPOTHYROXINEMIA
Normal TSH FT4
1-2% pregnancies
No adverse effects in pregnancy
No benefit of levothyroxine t/t
23. LAB TESTS & SCREENING
TSH
FT4
Antithyroid ab (Anti TPO & antithyroglobulin)
Case finding approach rather than universal screening
TSH should be done ideally before pregnancy
If not done, high risk women should be screened –
• Strong family history
• Autoimune disorder
• Presence of goiter
• Personal history of thyroid disease
• Therapeutic neck irradiation
• Medications
24. MANAGEMENT
Prepregnancy: 1.7μg/kg levothyroxine started
During pregnancy:
4-6wks
TSH normalized
Pregnancy
• If TSH > 5μU/ml start t/t
• If TSH 2.5-5μU/ml & AMA positive start t/t
• If TSH 2.5-5μU/ml & AMA negative monitor
closely
26. LEVOTHYROXINE SODIUM
Most widely prescribed t/t
Category A
25-300 mcg
If newly diagnosed in pregnancy started @ 1-2μg/kg/d
or approx 100-150μg/d
If previously hypothyroid dose increased by 25-40%
Taken empty stomach
Separated from multivitamins, calcium, iron, soy
products by 4hrs
Postpartum:
• Decrease dose by 30% (if newly diagnosed)
• Prepregnancy dose (known case)
• Reassess after 6 weeks
27. Adverse effect
On mother – Hyperthyroidism
Transient hair loss
BMD
Myocardial effects
On Fetus – LBW
Smaller HC
LABOR & DELIVERY-
• Should be euthyroid clincally & biochemically
• Stillbirth, preterm, preeclampsia, abruption
POSTPARTUM-
• Return to prepregnant dose
• Breast feeding is not contraindicated
28. NEONATAL HYPOTHYROIDISM
M/c endocrinopathies
Causes: Primary, secondary, tertiary.
Cord blood at birth OR heel prick on 3rd day
Symptoms & Signs
Goal – To normalize TSH(<5mU/l) & T4 (10-16μg/dl) as quickly as
possible.
3rd trim fetal T4 req : 6μg/kg/d
M/m-
• In utero: Intraamniotic 250-500μg thyroxine 7-10d interval
• In term infants: 10-15μg/kg/d
43. LABOR & DELIVERY
Antithyroid drugs
Beta blockers
Supportive care
Fetal thyrotoxicosis T/t of maternal thyrotoxicosis
Fetal goiter consider mode of delivery
EXIT procedure:
• Ex utero intrapartum treatment
• Fetus with large neck masses causing airway obstruction
44. POSTPARTUM MANAGEMENT
Immunosupression disappears
Relapse in 70 %
TSH & freeT4 done 6weeks post partum
Lactating mother-
• PTU & methimazole excreted in breast milk
• PTU protein bound. Safer
• Methimazole only at low doses (10-20mg/d)
45. THYROID STORM
Acute exacerbation of hyperthyroidism, life threatening,
hypermetabolic state
Rare in pregnancy
Pregnant women with thyrotoxicosis has minimal
cardiac reserve
Decompensation precipitated by sepsis, preeclampsia &
anemia
Features
Lab tests- increased T4 & T3, TLC, Transaminases,
calcium
Management..
46. START THIONAMIDES & CONTROL HEART RATE(<90bpm)
PTU 1g PO or NGT
100mg 6hrly
PROPRANOLOL 1-2mg IV over
5min to total 6-10mg
60-80mg 4hrly PO/NGT
CORTICOSTEROIDS
Dexa 1-2mg PO/IV/IM 6hrly
Or
Hydrocort 100mg IV 8hrly
Or
Prednisone 60mg/d PO
IODINE (after 1-2hrs of thionamide)
Sodium iodide 500-1000mg IV 8hrly
Or
SSKI 5drops PO 8hrly
Or
Lugol’s solution 10 drops PO 8hrly
Or
Lithium carbonate 300mg PO 6hrly
Or
iodinated radiocontrast agents iopodate 0.5-1g PO per day
47. THYROID CANCER IN PREGNANCY
Types: Papilllary (m/c in pregnancy), follicular,
medullary, Hurthle cell, anaplastic
Excellent long term prognosis
Surgery delayed postpartum
Sr. thyroglobulin- tumor marker
Postsurgical whole body scintigraphy & radioiodine
remnant ablation – contraindicated in pregnancy &
lactation
48. PRECONCEPTIONAL COUNSELLING
Clinical situations
Hyperthyroidism under t/t-
• Side effects of antithyroid drugs on fetus
• Wait 6mth after radioablation (4mth at least)
• Euthyroid at time of conception
Previous ablation for Grave’s disease-
• The dose needs to be increased soon after conception
• High maternal titers of TSI may be present in spite of euthyroid ; fetus at risk
Previous t/t for thyroid carcinoma
• Wait 1 yr after completion of radioactive t/t for conception.
Inadequate t/t
• Central congenital hypothyroidism in infant
49. POSTPARTUM THYROIDITIS
Rebound autoimmunity lymphocytic infilteration of gland
High chances(40-50%) if high titers of ab in early pregnancy
Anti- TPO 90% with PPT
Type 1 diabetics- 18-25% chances
20-50% will develop permanent hypothyroidism within 2-10yrs
Phases-
Hyperthyroid
Hypothyroid
50. HYPERTHYROID PHASE
• Release of stored
hormone
• 1-4mth postpartum
• Self limiting
• Abrupt onset
• Fatigue,palpitation,
insomnia,nervousness
• Small painless goiter
HYPOTHYROID PHASE
• Loss of functioning
thyrocytes
• 3-8mth
• Lasts longer
• Fatigue, wt gain,
depression, loss of conc.
51. THYROID NODULE IN PREGNANCY
95% of solitary thyroid nodule benign
Malignant- >4cm, firm to hard, lymph nodes, local invasion
Investigations-
• TSH
• FNAC
• USG
• Thyroid scan(contraindicated in pregnancy)
Editor's Notes
15 – 20 mm lateral lobes in breadth & isthmus,
Strctrl & fnctnl unit follicle contain thyroglobulin store t3 t4…. c cells secrete calcitonin… L thyroxine/ tetraiodothyronine, L-triiodothyronine
Trapping active transport by na+ k+ symport , oxidation occurs with peroxidase.. iodination occurs in thyroglobulin form MIT, DIT, coupling lead to formation T3 T4, T4 enters circulation by direct secretion & T3 produced by mono deiodination of T4 in periphery….thyroid is only source of T4… 20% of t3 ………..protein bound, thyroxine binding globuin (TBG) affinity for T4 major determinant in binding, transthyretin (TTR) 15% of T4 doesnot bind T3, albumin
Free active form available to tissue…
Placenta contains type 3 deiodinase
Primary..inadequate production despite pituitary stimulation eg iodine def
Sec…inadq stimulation by pituitary hth
Subclinical..asymptomatic increase tsh normal ft4
Overt..increase tsh low thyroxine symptomatic
Lithium amiodarone
There is little evidence whether there is benefit frm treating subclinical hypo & whether dis offsets risk of overt/t
Myxedema coma hypothermia bradycardia altered consciousness decreased deep tendon reflexes hyponatremia hypoglycemia hypoxia hypercapnia
Immediate supportive care & thyroid hormone replacement improves symptoms within 12 to 24 hrs of therapy 20% mortality
Patient can undertake pregnancy
If >5 t/t shud b started irrespective of clinical condition & antibodies
Profound myocardial effects like dilated cardiomyopathy can cause pulm htn & heart failure
Obstetric complications like…shud b kept in mind
Primary..thyroid agenesis or hypoplasia thyroid ectopy, dyshormonogenesis, endemic iodine deficiency, goitrogens, drug induced amiodarone, lithium, ki thioamides
Secondary pituitary causes tertiary hypothalamic causes
Bcoz of physiological tsh surge after birth
Symp..lethargy feedin diff constipation signs..growth retardation puffy eyes brady dry ruf skin prolonged relaxation DTR
Tab crushed n fed directly
When fetal lymphocytes enter matrnl circulation dey can live >20yrs
Thyrotropin binding inhibitory immunogb
Excess thyroid hormone production by overactive gland
Normal preg simulates Sum clinical findings similar to t4 excess so mild thyrotoxicosis may b difficut to diagnose
Subclinical hyperthyroidism no adverse effects on pregnancy not to b treated..long term may lead to osteoporosis, cardiovascular abn overt thyrotoxicosis &thyroid failure
Goal is to normalize & not to supress thyroid hormone & secondarily to treat symptoms
Aspirin displaces thyroid hormone from TBG & increases free hormone conc.
Fever or soar throat develops discontinue drug immediately
Clinical examntn for fetal growth
Usg for bradycardia growth parameters fetal goiter(symmeteric para tracheal mass neck hyperxtnsn poly)
Selective fetal sampling in previous I131 ablation, abnormal TSI or TBII, growth retardation, heart failure, goiter
Fetal thyroid destruction can occur wid RAiA
Elective cs to avoid dystocia
Ex utero intrapartum treatment procedure involves securing neonatal airway usually with endotracheal tube using laryngoscope while umbilical cord & maternal –fetal circulation remain intact to avoid difficult emergency intubation in delivery rum
Fever tachy wid atrial fibrillation, nausea vomit diarrhea dehydration, agitation delirium coma, high output cardiac failure, jaundice, abd pain