http://ebook2book.ir/ USMLE® STEP 2 CK: OBSTETRICS AND GYNECOLOGY Lecture Notes http://ebook2book.ir/ 2019 http://ebook2book.ir/ Table of Contents USMLE Step 2 CK Lecture Notes 2019: Obstetrics and Gynecology Cover Title Page Copyright Editor Feedback Page Part I: Obstetrics Chapter 1: Reproductive Basics Placental Hormones Physiologic Changes in Pregnancy Physiology of Lactation Embryology and Fetology Perinatal Statistics and Terminology Genetic Disorders Chapter 2: Failed Pregnancy Induced Abortion Early Pregnancy Bleeding Fetal Demise Ectopic Pregnancy Chapter 3: Obstetric Procedures Obstetrical Ultrasound Invasive Procedures Prenatal Diagnostic Testing Chapter 4: Prenatal Management of the Normal Pregnancy Diagnosing Pregnancy Establishing Gestational Age Identifying Prenatal Risk Factors Normal Pregnancy Events Normal Pregnancy Complaints Safe and Unsafe Immunizations Chapter 5: Prenatal Laboratory Testing First Trimester Laboratory Tests Second Trimester Laboratory Tests Third-Trimester Laboratory Tests http://ebook2book.ir/ Chapter 6: Late Pregnancy Bleeding Late Pregnancy Bleeding Chapter 7: Perinatal Infections Nonsexually Transmitted Sexually Transmitted Chapter 8: Obstetric Complications Cervical Insufficiency Multiple Gestation Alloimmunization Preterm Labor Premature Rupture of Membranes Post-term Pregnancy Chapter 9: Hypertensive Complications Hypertension in Pregnancy Gestational Hypertension Preeclampsia Preeclampsia with Severe Features Eclampsia Chronic Hypertension with or without Superimposed Preeclampsia HELLP Syndrome Chapter 10: Medical Complications in Pregnancy Cardiac Disease Thyroid Disease Seizure Disorders Diabetes Anemia Liver Disease Urinary Tract Infections Thrombophilias Antiphospholipid Syndrome Chapter 11: Disproportionate Fetal Growth Intrauterine Growth Restriction Macrosomia Chapter 12: Antepartum Fetal Testing Overview Nonstress Test Amniotic Fluid Assessment Biophysical Profile (BPP) http://ebook2book.ir/ Contraction Stress Test Umbilical Artery Doppler Chapter 13: Fetal Orientation in Utero Orientation in Utero Chapter 14: Normal and Abnormal Labor Overview of Labor Stages of Labor Conduct of Normal Spontaneous Labor Abnormal Labor Obstetric Complications During Labor Chapter 15: Obstetric Anesthesia Physiology Anesthetic Options During Labor Chapter 16: Intrapartum Fetal Monitoring Fetal Heart Rate Monitoring Intrapartum Fetal Heart Rate Monitoring Intrauterine Resuscitation Fetal pH Assessment Category III: Abnormal Tracings Chapter 17: Operative Obstetrics Operative Obstetrics Vaginal Birth After Cesarean (VBAC) External Cephalic Version Chapter 18: Postpartum Issues Postpartum Physiologic Issues Postpartum Contraception and Immunizations Postpartum Hemorrhage Postpartum Fever Part II: Gynecology Chapter 1: Basic Principles of Gynecology Female Reproductive Anatomy Gynecologic Procedures Chapter 2: Pelvic Relaxation Pelvic Organ Prolapse Vaginal Prolapse Urinary Incontinence Chapter 3: Disorders of the Vagina and Vulva Vaginal Discharge Vulvar Diseases http://ebook2book.ir/ Chapter 4: Disorders of the Cervix and Uterus Cervical Lesions Cervical Neoplasia Müllerian Anomalies Enlarged Uterus Endometrial Neoplasia Chapter 5: Disorders of the Ovaries and Oviducts Physiologic Enlargement Prepubertal Pelvic Mass Premenopausal Pelvic Mass Painful Adnexal Mass Postmenopausal Pelvic Mass Chapter 6: Gestational Trophoblastic Neoplasia Gestational Trophoblastic Neoplasia Chapter 7: Sexually Transmitted Diseases Spectrum of Organisms STDs with Ulcers STDs without Ulcers Hepatitis B Virus (HBV) Human Immunodeficiency Virus (HIV) Chapter 8: Pelvic Pain Pelvic Inflammatory Disease Primary Dysmenorrhea Secondary Dysmenorrhea Chapter 9: Fertility Control Fertility Control Barrier-Spermicidal Methods Steroid Contraception Intrauterine Contraception Long-Acting Reversible Contraception Natural Family Planning—Periodic Abstinence Coitus Interruptus Vaginal Douche Lactation Sterilization Chapter 10: Human Sexuality Human Sexual Response Cycle Sexual History-Taking Sexual Dysfunction http://ebook2book.ir/ Sexual Assault Chapter 11: Menstrual Abnormalities Menstrual Physiology Premenarchal Vaginal Bleeding Abnormal Vaginal Bleeding Primary Amenorrhea Secondary Amenorrhea Chapter 12: Hormonal Disorders Precocious Puberty Premenstrual Disorders Hirsutism Polycystic Ovarian Syndrome Infertility Menopause Chapter 13: The Female Breast Normal Breast Development Benign Breast Disorders Breast Cancer http://ebook2book.ir/ USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME), neither of which sponsors or endorses this product. This publication is designed to provide accurate information in regard to the subject matter covered as of its publication date, with the understanding that knowledge and best practice constantly evolve. The publisher is not engaged in rendering medical, legal, accounting, or other professional service. If medical or legal advice or other expert assistance is required, the services of a competent professional should be sought.
This publication is not intended for use in clinical practice or the delivery of medical care. To the fullest extent of the law, neither the Publisher nor the Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. © 2018 by Kaplan, Inc. Published by Kaplan Medical, a division of Kaplan, Inc.
750 Third Avenue New York, NY 10017 All rights reserved under International and Pan-American Copyright Conventions. By payment of the required fees, you have been granted the non-exclusive, non-transferable right to access and read the text of this eBook on screen. No part of this text may be reproduced, transmitted, downloaded, decompiled, reverse engineered, or stored in or introduced into any information storage and retrieval system, in any form or by any means, whether electronic or mechanical, now known or hereinafter invented, without the express written permission of the publisher. ISBN-13: 978-1-5062-3627-8 http://ebook2book.ir/ EDITOR Elmar Peter Sakala, MD, MA, MPH, FACOG Professor of Gynecology and Obstetrics Division of Maternal Fetal Medicine Department of Gynecology and Obstetrics Loma Linda University School of Medicine Loma Linda, CA http://ebook2book.ir/ CONTRIBUTORS Joshua P.
Kesterson, MD Assistant Professor Division of Gynecologic Oncology Department of Gynecology and Obstetrics Penn State College of Medicine Hershey, PA Alvin Schamroth, MD, FACOG Bethesda, MD http://ebook2book.ir/ We want to hear what you think. What do you like or not like about the Notes? Please email us at medfeedback@kaplan. http://ebook2book.ir/ Part I http://ebook2book.ir/ OBSTETRICS http://ebook2book.ir/ REPRODUCTIVE BASICS http://ebook2book.ir/ LEARNING OBJECTIVES Describe the basic physiology of spermatogenesis, ovulation, pregnancy, and lactation List the stages of fetal development and risks related to premature birth Answer questions about the terminology and epidemiology of perinatal statistics and genetic disorders detectable at birth http://ebook2book.ir/ PLACENTAL HORMONES HUMAN CHORIONIC GONADOTROPIN Human chorionic gonadotropin (hCG) is produced by the placental syncytiotrophoblast and first appears in maternal blood 10 days after fertilization. It peaks at 9–10 weeks and then gradually falls to a plateau level at 20–22 weeks.
By chemical structure hCG is a glycoprotein with 2 subunits. The α-subunit is similar to luteinizing hormone (LH), follicle-stimulating hormone (FSH), and thyrotropin (TSH). The β-subunit is specific for pregnancy. http://ebook2book.ir/ OB TRIAD Human Chorionic Gonadotropin (hCG) Produced by syncytiotrophoblast Similar to LH, FSH, & TSH Maintains corpus luteum The functions of hCG are as follows: Maintain corpus luteum production of progesterone until the placenta can take over maintenance of the pregnancy Regulate steroid biosynthesis in the placenta and fetal adrenal gland as well Stimulate testosterone production in the fetal male testes If hCG levels are high, twin pregnancy, hydatidiform mole, choriocarcinoma, or embryonal carcinoma can occur.
If levels are low, ectopic pregnancy, threatened abortion, or missed abortion can occur. http://ebook2book.ir/ HUMAN PLACENTAL LACTOGEN Human placental lactogen is chemically similar to anterior pituitary growth hormone and prolactin. Its level parallels placental growth, rising throughout pregnancy. http://ebook2book.ir/ OB TRIAD Human Placental Lactogen (hPL) Produced by syncytiotrophoblast Similar to HGH, prolactin Decreases insulin sensitivity Its effect is to antagonize the cellular action of insulin, decreasing insulin utilization and thereby contributing to the predisposition of pregnancy to glucose intolerance and diabetes.
If levels are low, threatened abortion or intrauterine growth restriction (IUGR) can occur. http://ebook2book.ir/ PROGESTERONE Progesterone is a steroid hormone produced after ovulation by the luteal cells of the corpus luteum to induce endometrial secretory changes favorable for blastocyst implantation. It is initially produced exclusively by the corpus luteum for up to 6–7 menstrual weeks. Between 7–9 weeks, both the corpus luteum and the placenta produce progesterone.
After 9 weeks the corpus luteum declines, and progesterone is exclusively produced by the placenta. http://ebook2book.ir/ OB TRIAD Progesterone Produced by corpus luteum Prepares endometrium for implantation Decreased myometrial contractility The functions of progesterone are as follows: In early pregnancy it induces endometrial secretory changes favorable for blastocyst implantation. In later pregnancy its function is to induce immune tolerance for the pregnancy and prevent myometrial contractions. http://ebook2book.ir/ ESTROGEN Estrogens are steroid hormones that occur in 3 forms.
Each form has unique significance during a woman’s life. Estradiol is the predominant moiety during the nonpregnant reproductive years. It is converted from androgens (produced from cholesterol in the follicular theca cells), which diffuse into the follicular granulosa cells containing the aromatase enzyme that completes the transformation into estradiol. Estriol is the main estrogen during pregnancy.
Dehydroepiandrosterone- sulfate (DHEAS) from the fetal adrenal gland is the precursor for 90% of estriol converted by sulfatase enzyme in the placenta. Estrone is the main form during menopause. Postmenopausally, adrenal androstenedione is converted in peripheral adipose tissue to estrone. Estradiol Nonpregnant reproductive years Follicle Granulosa Estriol Pregnancy Placenta from fetal adrenal DHEAS Estrone After menopause Adipose from adrenal steroids Table I-1-1.
Estrogens Throughout a Woman’s Life http://ebook2book.ir/ PHYSIOLOGIC CHANGES IN PREGNANCY SKIN Striae gravidarum: “stretch marks” that develop in genetically predisposed women on the abdomen and buttocks Spider angiomata and palmar erythema: caused by increased skin vascularity Chadwick sign: bluish or purplish discoloration of the vagina and cervix caused by increased skin vascularity Linea nigra: increased pigmentation of the lower abdominal midline from the pubis to the umbilicus Chloasma: blotchy pigmentation of the nose and face http://ebook2book.ir/ CARDIOVASCULAR Arterial blood pressure: Systolic and diastolic values both decline early in the first trimester, reaching a nadir by 24–28 weeks and then gradually rising toward term (but never returning quite to prepregnancy baseline). Diastolic falls more than systolic, as much as 15 mm Hg. Arterial blood pressure is never normally elevated in pregnancy. Venous blood pressure: Central venous pressure (CVP) is unchanged with pregnancy, but femoral venous pressure (FVP) increases two- to threefold by 30 weeks' gestation.
Plasma volume: Plasma volume increases up to 50% with a significant increase by the first trimester. Maximum increase is by 30 weeks. This increase is even greater with multiple fetuses. Systemic vascular resistance (SVR): SVR equals blood pressure (BP) divided by cardiac output (CO).
Because BP decreases and CO increases, SVR declines by 30%, reaching its nadir by 20 weeks. This enhances uteroplacental perfusion. Cardiac output (CO): CO increases up to 50%, with the major increase by 20 weeks. CO is the product of heart rate (HR) and stroke volume (SV), and both increase in pregnancy.
HR increases by 20 beats/min by the third trimester. SV increases by 30% by the end of the first trimester. CO is dependent on maternal position. CO is lowest in the supine position because of inferior vena cava compression resulting in decreased cardiac return.
CO is highest in the left lateral position. CO increases progressively through the three stages of labor. http://ebook2book.ir/ Murmurs: A systolic ejection murmur along the left sternal border is normal in pregnancy, owing to increased CO passing through the aortic and pulmonary valves. Diastolic murmurs are never normal in pregnancy and must be investigated.
Arterial blood pressure Systolic ↓ Diastolic ↓↓ Venous pressure Central Unchanged Femoral ↑ Peripheral vascular resistance ↓ Table I-1-2. Cardiovascular Changes http://ebook2book.ir/ HEMATOLOGIC Red blood cell (RBC) mass increases by 30% in pregnancy; thus, oxygen- carrying capacity increases. However, because plasma volume increases by 50% the calculated hemoglobin and hematocrit values decrease by 15%. The nadir of the hemoglobin value is at 28–30 weeks' gestation.
This is a physiologic dilutional effect, not a manifestation of anemia. White blood cell (WBC) count increases progressively during pregnancy, with a mean value of up to 16,000/mm3 in the third trimester. Erythrocyte sedimentation rate (ESR) increases in pregnancy because of the increase in gamma globulins. Platelet count normal reference range is unchanged in pregnancy.
Coagulation factors: Factors V, VII, VIII, IX, XII, and von Willebrand factor increase progressively in pregnancy, leading to a hypercoagulable state. http://ebook2book.ir/ GASTROINTESTINAL Stomach: Gastric motility decreases and emptying time increases from the progesterone effect on smooth muscle. This increase in stomach residual volume, along with upward displacement of intraabdominal contents by the gravid uterus, predisposes to aspiration pneumonia with general anesthesia at delivery. Large bowel: Colonic motility decreases and transit time increases from the progesterone effect on smooth muscle.
This predisposes to increased colonic fluid absorption, resulting in constipation. http://ebook2book.ir/ PULMONARY Tidal volume (Vt), the volume of air that moves in and out of the lungs at rest, increases with pregnancy to 40%.