Venous thromboembolism (VTE), which includes deep vein thrombosis and pulmonary embolism, can occur during pregnancy. The risk of VTE is highest during the antepartum period and with cesarean delivery. Risk factors include prior VTE, thrombophilia, older age, obesity, multiparity, bed rest, and certain medical conditions. Treatment involves anticoagulants like heparin and warfarin, with heparin preferred in early pregnancy due to risks of warfarin exposure to the fetus. Patients are classified as very high, high, moderate, or low risk, with treatment strategies varying based on risk level.
Lecture by Dr Sujoy Dasgupta in BOGSCON 2015, the Annual Conference of Bengal Obstetric and Gynaecological Society, held at Hotel Novotel, Kolkata in January, 2015; where he had been invited as FACULTY to deliver his lecture
Lecture by Dr Sujoy Dasgupta in BOGSCON 2015, the Annual Conference of Bengal Obstetric and Gynaecological Society, held at Hotel Novotel, Kolkata in January, 2015; where he had been invited as FACULTY to deliver his lecture
Sickle cell anemia is an autosome linked recessive trait that can be transmitted from parents to the offspring when
both the partners are carrier for the gene (or heterozygous). The disease is controlled by a single pair of allele, HbA
and HbS. Out of the three possible genotypes only homozygous individuals for HbS (HbS, HbS) show the diseased phenotype. The ability to predict the clinical course of SCD during pregnancy is difficult. It is mandatory to follow up the patient closely from the very beginning i.e. from preconception to antenatal till labor. SCD is associated with both maternal and fetal complications and is associated with an increased incidence of perinatal mortality, premature
labor, fetal growth restriction and acute painful crises during pregnancy.
Sickle cell anemia is an autosome linked recessive trait that can be transmitted from parents to the offspring when
both the partners are carrier for the gene (or heterozygous). The disease is controlled by a single pair of allele, HbA
and HbS. Out of the three possible genotypes only homozygous individuals for HbS (HbS, HbS) show the diseased phenotype. The ability to predict the clinical course of SCD during pregnancy is difficult. It is mandatory to follow up the patient closely from the very beginning i.e. from preconception to antenatal till labor. SCD is associated with both maternal and fetal complications and is associated with an increased incidence of perinatal mortality, premature
labor, fetal growth restriction and acute painful crises during pregnancy.
Primary Maternal Care: Hypertensive disorders of pregnancySaide OER Africa
Primary Maternal Care addresses the needs of healthcare workers in level 1 district hospitals and clinics who provide antenatal and postnatal care, but do not conduct deliveries. It is adapted from theory chapters and skills workshops from Maternal Care. This book complements the national protocol of antenatal care in South Africa. It covers: booking for antenatal care, assesing fetal growth and wellbeing, hypertensive disorders of pregnancy, antepartum haemorrhage, preterm labour, important medical conditions
The Diagnostic Value of Saline Infusion Sonohysterography Versus Hysteroscopy...Ahmed Mowafy
The Diagnostic Value of Saline Infusion Sonohysterography Versus Hysteroscopy in Evaluation of Uterine Cavity in Patients with Infertility and Recurrent Pregnancy Loss
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.
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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
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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.
Maxilla, Mandible & Hyoid Bone & Clinical Correlations by Dr. RIG.pptx
Venous thromboembolism during pregnancy
1. `
VENOUS THROMBOEMBOLISM DURING PREGNANCY
1A-MOWAFY 2013
VTE = Venous thromboembolism
Includes; Deep venous thrombosis DVT, Pulmonary embolism PE
INCIDENCE :
2-3 in 1000 pregnancies
DVT 80% PE 20%
2/3 of DVT are antepartum
Caesarean section increases the risk 3-5 fold than vaginal delivery
PATHOGENESIS
Virchow’s triade =
1. Circulatory stasis
2. Vascular damage
3. Increased blood co-agulation
AETIOLOGY
Risk factors:
1. Pregnancy itself is a risk factor
2. Previous VTE in patient on hormonal contraception
3. Previous VTE during pregnancy ( risk is 12 % )
4. Rheumatic heart disease and patients with heart prosthesis
5. Thrombophilias (congenital and acquired?!)
6. Age ˃ 35 years old
7. Obesity ; BMI ˃ 30
8. Multiparity ; parity ˃ 4
9. Recurrent miscarriage
10. Bed rest and physical immobility
11. Hyperemesis gravidarum
12. Shock and dehydration
13. Infections
Venous thromboembolism
during pregnancy
Venous thromboembolism during pregnancy
2. `
VENOUS THROMBOEMBOLISM DURING PREGNANCY
2A-MOWAFY 2013
14. Pregnancy-induced hypertension
15. Excessive blood loss
16. Prolonged labour
17. Instrumental delivery
18. Cesarean section
19. Pelvic surgery in peri-partum period
20. Sickle cell anemia
21. Gross varicose veins
22. Fetal demise with remaining viable fetus
23. Intra-uterine gross restriction IUGR
Q: What is thrombophilia?
It is abnormalities in the blood co-agulation that is increases the risk of thrombosis;
(congenital, Acquired?)
3. `
VENOUS THROMBOEMBOLISM DURING PREGNANCY
3A-MOWAFY 2013
RISKY GROUPS AND THEIR MANAGEMENT:
Very high risk
Criteria Previous VTE with thrombophilia
Long term warfarin therapy
Antepartum High prophylactic dose or therapeutic dose of LMWH
Postpartum LMWH for 5 days + Warfarin
High risk
Criteria Previous recurrent VTE
VTE once with thrombophilia
VTE once with positive family history
Diagnosed important thrombophilia
Valvular mechanical prosthesis
Antepartum prophylactic dose LMWH
Postpartum LMWH for 5 days + Warfarin for 6 weeks
Moderate risk
Criteria Single provoked VTE without thrombophilia
Thrombophilia + Anti-thrombin III deficiency
Mitral stenosis
Antepartum Antenatal aspirin
Postpartum LMWH for 5 days + Warfarin for 6 weeks
Low risk
Criteria Two or more of the following :
Obesity
Age ˃ 35
Parity ˃ 4
Gross varicose veins
Recurrent hypertensive disorders
Antepartum Antenatal aspirin
Postpartum Warfarin for 6 weeks
4. `
VENOUS THROMBOEMBOLISM DURING PREGNANCY
4A-MOWAFY 2013
ANTI-COAGULANT DRUGS:
Heparin
Types I. Unfractionated heparin → UFH “Cal-heparin”
II. Low molecular weight heparin → LMWH “Clexan”
Onset Within 10 minutes
Half-life 6 hours
Doses
I. Unfractionated heparin
Normal body weight → 5000 IU/day
Body weight ˂ 50 kg → 2500 IU/day
Body weight ˃ 90 kg → 5000 IU/12 h
High prophylactic dose→ 100 IU/kg/12h
II. Low molecular weight heparin
Normal body weight → 40 mg/day
Body weight ˂ 50 kg → 20 mg /day
Body weight ˃ 90 kg → 40 mg / 12h
High prophylactic dose→ I mg/kg/12h
Monitoring 1. Activated partial thromboplastin aPPT twice weekly
2. Plattlets concentration monthly
3. Bone mineral density every 3 months
Advantages
1. No effect on the fetus ( does not cross placental blood barrier )
2. Not secreted on milk ( no effect on lactation )
N.B : advantages of LMWH over UFH
o Fewer side effect
o Prolonged half-life
o Greater inhibitory effect on factor X
o Prophylactic dose once daily
o No need for continuous laboratory monitoring
Drawbacks Increase bleeding tendency
Osteoporosis ( improved by adding calcium , hence name “ Cal-heparin “
Fat necrosis at site of injection
Alopecia
Anti-dot Protamine sulphate 1mg/100IU
5. `
VENOUS THROMBOEMBOLISM DURING PREGNANCY
5A-MOWAFY 2013
Oral anti-coagulant drugs
Types I. Coumarine → Warfarin sodium “Marevan”
II. Indandione → phenoidione “Dindevan”
Onset Full effect after 5 days
Half-life Warfarin → 44 hours
Phenoidione → 5 hours
Doses 2 to 5 mg/day
Monitoring 1. INR = “ international randomized ratio “→ should be 2 to 3
2. PT = “ prothrombine time “→ 30–50 % of normal control
Advantages Oral route , potent and long acting
Drawbacks Maternal :
1. Skin: allergy, fever, rash, urticarial and dermatitis
2. Blood: agranulocytosis
3. Liver: liver disturbances; jaundice
4. Renal: renal disturbances; hematuria
5. Over dose → bleeding tendency
Fetal :
1. Warfarin embryopathy; nasal hypoplasia, depression of nasal bone, mental
retardation, optic atrophy, skeletal defect ‘ bone splitting’
2. Can cross placental-blood barrier; bleeding tendency and increases the risks
of intracranial hemorrhage and accidental hemorrhage
Drug interactions :
1. drugs increases the effect : salicylates, quinine, steroids
2. drugs decreases the effect : hepatic enzyme inducers
Anti-dot Vitamin K IM. , SC.
For rapid effect :
1. Fresh blood , fresh frozen plasma
2. Vitamin K to the mother and baby
PROTOCOLS FOR ANTI-COAGULATION DURING PREGNANCY
Frist trimester → only heparin for fear of warfarin embryopathy
Second trimester → warfarin starting from 13 weeks
Continue till:
33 weeks if risk of preterm laobour exist
36 weeks if no risk of preterm labour
However, oral anti-coagulants are not absolutely safe as delayed warfarin
embryopathy is recorded
Late in pregnancy: at 33 – 36 weeks → shift to heparin again
Postpartum: Vitamin K to the mother and baby and readjust the dose