Essential Human Development E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: essentials
• Sprache: Englisch

Seitenzahl: 1220

Veröffentlichungsjahr: 2018

Beschreibung

As our understanding of the human body broadens, so does the need for a comprehensive text that encompasses all aspects of human development. Essential Human Development is a great course companion that focuses on the human life cycle, ideal for the undergraduate student new to these fields, or for qualified practitioners looking for a reference guide.

Featuring key information points and self-test assessments in each chapter, the book is organised in an accessible manner, beginning with fertilisation and embryology, then moving on to obstetric medicine, neonatal care and child health, with the final section exploring gynaecological medicine.  

Ensuring that information is placed in context to aid understanding, Essential Human Development is the perfect support for the modern medical school curriculum, as well as a vital reminder of the core information needed whilst on a women or child health clinical placement.

Leseprobe

CONTENTS

Cover

Title Page

Copyright

List of Contributors

Preface

How to Use Your Textbook

About the Companion Website

Part 1: Fertilisation

Chapter 1: Principles of Development

Case

Chromosomes

Mitosis

Meiosis

Spermatogenesis

Oogenesis

Growth

Differentiation

Signalling

Organisation

Morphogenesis

Chapter 2: The Female Reproductive System

Case

Anatomy

Physiology

Chapter 3: The Male Reproductive System

Case

Anatomy

Embryology

Physiology

Chapter 4: Fertilisation

Case

Anatomy

Cell Biology

Physiology of Fertilisation and the Endometrium

Chapter 5: Embryology: Zygote to Blastocyst

Case

Zygote

Decidualisation

Implantation

Placenta

Sacs of the Embryo

Chapter 6: Embryonic Stem Cells

Case

Embryonic Stem Cells

Stem Cells in Medicine

Ethical Arguments

Law

Part 2: Pregnancy

Chapter 7: Embryology

Case

Embryological Development

Gastrulation

Embryology of the Gastrointestinal System

Neuroembryology

Cardiovascular Embryology

Respiratory Embryology

Musculoskeletal Embryology

Urogenital Embryology

Chapter 8: Physiology of Pregnancy

Case

Systemic Changes During Pregnancy

Chapter 9: Antenatal Care

Case

Assessment of Risk

History

Examination and Investigations

Chapter 10: Antenatal Screening and Prenatal Diagnosis

Case

Obstetric Ultrasound Screening for Fetal Anomaly

Screening for Chromosomal Anomalies

Invasive Tests

Infection in Pregnancy

Chapter 11: Hypertensive Disorders of Pregnancy

Case

Introduction

Definitions

Risks of Hypertension in Pregnancy

Pathology of Pre-Eclampsia and Eclampsia

Clinical Picture

Management

Care During Delivery

Care After Delivery

Chapter 12: Diseases in Pregnancy I

Case

Diabetes in Pregnancy

Chapter 13: Diseases in Pregnancy II

Case

Connective Tissue Disorders

Backache

Carpal Tunnel Syndrome

Hyperemesis Gravidarum

Gastroesophageal Reflux Disease (GORD)

Constipation

Haemorrhoids

Varicose Veins, Varicosities

Dermatological Conditions in Pregnancy

Psychiatric Disease in Pregnancy

Chapter 14: Multiple Pregnancy and Other Antenatal Complications

Case

Incidence of Twins and Chorionicity

Identification of Twin Conception

Risks to the Fetus

Risks to the Mother

Chapter 15: Problems in Late Pregnancy

Case

Antepartum Haemorrhage

Placenta Praevia

Adherent Placenta

Abruptio Placentae

Vasa Praevia

Other Causes of Antepartum Haemorrhage

Reduced Fetal Movements

Prolonged Pregnancy

Chapter 16: Fetal Growth and Tests of Fetal Wellbeing

Case

Definition and Types of Fetal Growth Restriction

Diagnosis of Fetal Growth Restriction

Screening for Fetal Growth Restriction

Fetal Surveillance

Management of Fetal Growth Restriction

Chapter 17: The Eye in Pregnancy and the Newborn

Case

Differential Diagnosis of Paediatric Leucocoria

Case

Introduction

Physiological Changes

Pregnancy-Specific Ocular Disease

Pre-Existing Ocular Disease During Pregnancy

Part 3: Birth

Chapter 18: Normal Labour

Case

Labour

Definitions

Mechanism of Normal Labour

Management of Labour

The Partogram and its Importance

Analgesia in Labour

Useful Drugs in Obstetrics and their Actions

Chapter 19: Abnormal Labour

Case

Definitions

Diagnosis

Causes of Abnormal Labour

Types of Abnormal Labour

Preterm Labour

Prevention and Prediction of Preterm Labour

Induction of Labour

Chapter 20: The Puerperium

Case Study

Physiological Changes

Postnatal Care

Psychological Wellbeing

Lactation and Breastfeeding

Secondary Postpartum Haemorrhage (PPH)

Sepsis

Thrombotic Conditions

Peripartum Cardiomyopathy

Chapter 21: Obstetric Emergencies

Case

Initial Management of Obstetric Emergencies

Causes of Maternal Collapse

Massive Obstetric Haemorrhage

Venous Thromboembolism

Shoulder Dystocia

Cord Prolapse

Amniotic Fluid Embolism

Uterine Inversion

Fetal Distress in the Second Twin

Part 4: Neonatology

Chapter 22: Newborn Resuscitation and Newborn Examination

Case

Newborn Resuscitation

Examination of the Newborn

Chapter 23: Newborn Feeding, Jaundice and Maternal Diabetes

Case

Introduction

Breastfeeding

Formula Feeding

Vitamin K

Vitamin D

Weaning and Milk Feeding in Older Infants

Neonatal Jaundice

Haemolytic Disease of the Newborn (HDN)

Normal Growth and Maturity

Infants of Mothers with Diabetes

Chapter 24: The Preterm Infant

Case

Introduction

Preterm Labour

Antenatal Steroid Therapy

Care at Birth

Respiratory Distress Syndrome

Apnoea of Prematurity

Fluid Management and Nutrition

Patent Ductus Arteriosus

Bronchopulmonary Dysplasia (BPD)

Necrotising Enterocolitis (NEC)

Retinopathy of Prematurity (ROP)

Outcomes Following Extreme Preterm Birth

Discharge of the Preterm Baby From Hospital

Chapter 25: Congenital and Perinatal Infection

Case

Introduction

Congenital Infection

Cytomegalovirus (CMV)

Rubella

Toxoplasmosis

Syphilis

Other Viral Infections

Early-Onset Sepsis

Late-Onset Sepsis

Part 5: Childhood and Adolescence

Chapter 26: History and Examination in Childhood

Case

Introduction

The Paediatric History

The Paediatric Examination

Cardiovascular Examination

Respiratory Examination

Gastrointestinal Examination

Neurological Examination

Ear and Throat Examination

Skin and Musculoskeletal System

Chapter 27: Normal Growth and Developmental Milestones

Case

Growth

Physiology of Growth

Periods of Growth

Measuring Growth

Development

Chapter 28: Developmental Delay

Case

Normal Development

Developmental Delay

Assessing Development

Investigations

Education

Chapter 29: Genetics

Case

Introduction

Clinical Genetics and Genetic Tests

Ethics

Dysmorphology

Genetic Mutations

Genetic Disorders

Techniques Used for Genetic Testing

Chapter 30: Neurodevelopmental Disorders

Case

Learning Disability/Intellectual Disability (LD/ID)

Autism Spectrum Disorder (ASD)

Attention Deficit Hyperactivity Disorder (ADHD)

Developmental Coordination Disorder

Chapter 31: Puberty

Case History

Introduction

Normal Puberty

Assessment of Puberty

Abnormal Puberty

The Psychology of Adolescence

Adolescent Healthcare

Chapter 32: Non-Accidental Injury and Neglect

Case

Introduction

Incidence

Important Legislation

Vulnerable Groups

Types of Abuse

Actions Required if you are Concerned about a Child

Chapter 33: Neurological Problems

Case

Headache

Fits, Faints and Funny Turns

The Epilepsies

Cerebral Palsy

Neuromuscular Diseases in Children

Muscle Disorders

Neural Tube Defects and Hydrocephalus

Chapter 34: Infections and Immunodeficiency

Case

Measles

Mumps

Human Herpes Virus

Varicella Zoster (Chickenpox)

Epstein–Barr Virus (EBV)

Parvovirus B19

Meningitis and Meningococcal Septicaemia

Immune Deficiencies in Children

Chapter 35: Haematology and Oncology

Case

Introduction

Anaemia in Children

Iron Deficiency Anaemia (IDA)

Megaloblastic Anaemia

Anaemia Caused by Increased red Cell Destruction (Haemolytic Anaemia)

Bleeding Disorders

Oncology

Chapter 36: Congenital and Acquired Heart Disease

Case

The Fetal Circulation

Changes at Birth

Heart Disease in Children

Ventricular Septal Defect (VSD).

Other ‘Left-to-Right’ Heart Lesions

Pulmonary Stenosis (PS)

Coarctation of the Aorta

Aortic Stenosis

Cyanotic Heart Lesions

Tetralogy of Fallot

Transposition of the Great Arteries (TGA)

Total Anomalous Pulmonary Venous Connection

Tricuspid Atresia

Hypoplastic Left Heart Syndrome

Truncus Arteriosus

Arrhythmias

The Innocent Heart Murmur

Chapter 37: Metabolic and Endocrine Disorders

Case

Introduction to Endocrinology

Obesity

Diabetes Mellitus

Hypoglycaemia

The Thyroid Gland

Calcium Homeostasis

Hypocalcaemia

Hypercalcaemia

Parathyroid Disorders

Multiple Endocrine Neoplasias

Von Hippel–Lindau Syndrome

The Adrenal Gland

Hypopituitarism

Diabetes Insipidus

Syndrome of Inappropriate ADH

Metabolic Disease

Chapter 38: Respiratory Problems

Case

Introduction

Upper Airway Disorders

Bronchiolitis

Pneumonia

Cystic Fibrosis

Chapter 39: Gastroenterology, Nutrition and Faltering Growth

Case

Introduction

Vomiting

Malabsorption

Cow's Milk Protein Allergy (CMPA)

Post-Gastroenteritis Syndrome

Inflammatory Bowel Disease (IBD)

Gastroenteritis

Other Causes of Diarrhoea

Toddler Diarrhoea

Constipation

Abdominal Pain

Gastrointestinal Bleeding

Meckel's Diverticulum

Faltering Growth

Malnutrition

Chapter 40: Renal and Urinary Problems

Case

Urinary Tract Infections

Abnormalities of the Urinary Tract

Antenatal Detection of Renal Abnormalities

Haematuria

Glomerulonephritis

Henoch–Schönlein Purpura (HSP)

Proteinuria

Acute Renal Failure (ARF)

Chronic Renal Failure (CRF)

Hypertension

Chapter 41: Dermatology

Case

How to Describe Skin Lesions

Dermatological Conditions in Infants and Children

Inflammatory Skin Conditions

Bacterial Skin Infections

Viral Skin Infections

Skin Manifestations of Viral Illnesses

Fungal Skin Infections

Skin Infestations

Neonatal Skin Conditions

Hair Disorders

Skin Manifestations of Systemic Conditions

Bullous Skin Disorders

Chapter 42: Rheumatology and Orthopaedics

Case

Introduction

Paediatric Orthopaedic and Rheumatology Conditions

The Limping Child

Hip Conditions

Leg Pain

Back Pain

Fractures in Non-Accidental Injury (NAI)

Juvenile Idiopathic Arthritis (JIA)

Bone Tumours

Infections

Neonatal Problems

Inherited Disorders

Chapter 43: Paediatric Surgery

Case

Gastrointestinal Conditions

Urological Conditions

Chapter 44: Paediatric Pharmacology

Case

Introduction

Pharmacokinetics

Absorption and Administration

Distribution

Metabolism and Excretion

Pharmacodynamics

Intravenous Fluids

Calculating the Deficit in Dehydration

NPSA Alert (National Patient Safety Agency)

Part 6: Gynaecology

Chapter 45: Problems in Early Pregnancy

Case

Introduction

Embryology

Development of Placenta and Membranes

Relevant Endocrinology

Miscarriage

Ectopic Pregnancy

Hyperemesis Gravidarum

Gestational Trophoblastic Disease

Summary of Approach to Common Problems in Early Pregnancy

Chapter 46: Subfertility

Case

Introduction

History of Assisted Reproduction

Changing Reproductive Behaviour

Prevalence

The Hypothalamo-Pituitary-Gonadal Axis

Factors Affecting Fertility

Types of Subfertility

Chapter 47: Vaginal Discharge, Pelvic Pain and Endometriosis

Case

Vaginal Discharge

Endometriosis

Chapter 48: Termination of Pregnancy

Case

Introduction

Legal Considerations

Ethical Considerations

Termination for Fetal Abnormalities

Termination of Pregnancy: The Global View

Indications for Termination of Pregnancy

The Process for Termination of Pregnancy

Complications of Medical and Surgical Termination of Pregnancy

Common Physical Symptoms After Termination of Pregnancy (TOP)

Complications of TOP

Focus on Infection

Psychological Sequelae of Termination of Pregnancy

Chapter 49: Contraception

Case

Natural Family Planning (or ‘Rhythm Methods’)

Barrier Methods

Combined Oral Methods

Progesterone-Only Pills

Long-Acting Reversible Contraception (Larc)

Emergency/Postcoital Contraception

Sterilisation

Chapter 50: Obstetric and Gynaecological Operations

Case

Episiotomy

Operative or Assisted Vaginal Delivery

Caesarean Section

Hysteroscopy

Laparoscopy

Abdominal and Vaginal Hysterectomy

Surgical Prolapse Procedure

Uterovaginal Prolapse Surgeries

Surgery for Stress Incontinence

Chapter 51: The Menopause

Case

Introduction

History Taking

Investigations

Diagnosis

Premature Ovarian Failure (POF)

Resistant Ovarian Syndrome

Assessment of Women for Hormone Replacement Therapy (HRT)

Alternative Therapies

Further Reading

References

Index

End User License Agreement

List of Tables

Table 9.1

Table 10.1

Table 10.2

Table 10.3

Table 10.4

Table 10.5

Table 10.6

Table 10.7

Table 10.8

Table 10.9

Table 11.1

Table 11.2

Table 11.3

Table 12.1

Table 12.2

Table 12.3

Table 12.4

Table 13.1

Table 13.2

Table 13.3

Table 13.4

Table 13.5

Table 13.6

Table 15.1

Table 15.2

Table 15.3

Table 15.4

Table 15.5

Table 15.6

Table 16.1

Table 16.2

Table 17.1

Table 17.2

Table 17.2

Table 18.1

Table 18.2

Table 19.1

Table 19.2

Table 19.3

Table 22.1

Table 22.2

Table 23.1

Table 24.1

Table 25.1

Table 25.2

Table 26.1

Table 26.2

Table 27.1

Table 27.2

Table 27.3

Table 27.4

Table 27.5

Table 27.6

Table 27.7

Table 27.8

Table 28.1

Table 28.2

Table 28.3

Table 28.4

Table 28.5

Table 33.1

Table 33.1

Table 33.2

Table 33.3

Table 33.4

Table 33.5

Table 33.6

Table 33.7

Table 33.8

Table 33.9

Table 33.10

Table 34.1

Table 34.2

Table 34.3

Table 34.4

Table 35.1

Table 37.1

Table 37.2

Table 37.3

Table 37.4

Table 38.1

Table 38.2

Table 38.3

Table 38.4

Table 39.1

Table 39.2

Table 39.3

Table 39.4

Table 39.5

Table 39.6

Table 39.7

Table 39.8

Table 40.1

Table 40.2

Table 40.3

Table 40.4

Table 44.1

Table 44.2

Table 45.1

Table 45.2

Table 45.3

Table 45.4

Table 45.5

Table 45.6

Table 45.7

Table 45.8

Table 47.1

Table 47.2

Table 47.3

Table 48.1

Table 48.2

Table 49.1

Table 50.1

Table 51.1

List of Illustrations

Figure 1.1

Figure 1.2

Figure 1.3

Figure 1.4

Figure 1.5

Figure 1.6

Figure 1.7

Figure 2.1

Figure 2.2

Figure 2.3

Figure 2.4

Figure 2.5

Figure 2.6

Figure 2.7

Figure 2.8

Figure 2.9

Figure 2.10

Figure 2.11

Figure 2.12

Figure 2.13

Figure 2.14

Figure 3.1

Figure 3.2

Figure 3.3

Figure 3.4

Figure 4.1

Figure 4.2

Figure 4.3

Figure 4.4

Figure 5.1

Figure 5.2

Figure 5.3

Figure 5.4

Figure 6.1

Figure 6.2

Figure 6.3

Figure 7.1

Figure 7.2

Figure 7.3

Figure 7.4

Figure 7.5

Figure 7.6

Figure 7.7

Figure 7.8

Figure 7.9

Figure 8.1

Figure 8.2

Figure 9.1

Figure 9.2

Figure 10.1

Figure 14.1

Figure 14.2

Figure 15.1

Figure 15.2

Figure 15.3

Figure 16.1

Figure 16.2

Figure 16.3

Figure 16.4

Figure 17.1

Figure 17.2

Figure 17.3

Figure 17.4

Figure 17.5

Figure 17.6

Figure 17.7

Figure 17.8

Figure 17.9

Figure 17.10

Figure 17.11

Figure 17.12

Figure 17.13

Figure 17.14

Figure 17.15

Figure 17.16

Figure 18.1

Figure 18.2

Figure 18.3

Figure 18.4

Figure 19.1

Figure 19.2

Figure 19.3

Figure 19.4

Figure 19.5

Figure 20.1

Figure 20.2

Figure 21.1

Figure 21.2

Figure 21.3

Figure 21.4

Figure 21.5

Figure 22.1

Figure 22.2

Figure 22.3

Figure 22.4

Figure 22.5

Figure 22.6

Figure 22.7

Figure 23.1

Figure 24.1

Figure 26.1

Figure 26.2

Figure 26.3

Figure 27.1

Figure 27.2

Figure 27.3

Figure 28.1

Figure 28.2

Figure 29.1

Figure 29.2

Figure 29.3

Figure 29.4

Figure 31.1

Figure 31.2

Figure 31.3

Figure 31.4

Figure 32.1

Figure 32.2

Figure 32.3

Figure 33.1

Figure 33.2

Figure 33.3

Figure 33.4

Figure 33.5

Figure 34.1

Figure 34.2

Figure 34.3

Figure 34.4

Figure 34.5

Figure 34.6

Figure 35.1

Figure 35.2

Figure 35.3

Figure 35.4

Figure 35.5

Figure 36.1

Figure 36.2

Figure 36.3

Figure 36.4

Figure 36.5

Figure 36.6

Figure 36.7

Figure 36.8

Figure 36.9

Figure 37.1

Figure 37.2

Figure 37.3

Figure 37.4

Figure 37.5

Figure 37.6

Figure 37.7

Figure 38.1

Figure 39.1

Figure 39.2

Figure 39.3

Figure 39.4

Figure 39.5

Figure 39.6

Figure 39.7

Figure 40.1

Figure 40.2

Figure 40.3

Figure 40.4

Figure 41.1

Figure 41.2

Figure 41.3

Figure 41.4

Figure 41.5

Figure 41.6

Figure 41.7

Figure 41.8

Figure 41.9

Figure 42.1

Figure 42.2

Figure 43.1

Figure 43.2

Figure 43.3

Figure 43.4

Figure 43.5

Figure 43.6

Figure 45.1

Figure 45.2

Figure 46.1

Figure 46.2

Figure 46.3

Figure 46.4

Figure 46.5

Figure 49.1

Figure 49.2

Figure 50.1

Figure 50.2

Figure 50.3

Figure 50.4

Figure 50.5

Figure 50.6

Guide

Cover

Table of Contents

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Essential Human Development

Edited by

Samuel Webster

PhD, FHEA

Senior Lecturer in Anatomy & Embryology Swansea University Medical School Swansea, UK

Geraint Morris

MB, BCh, FRCPCH

Consultant Neonatologist and Clinical Director, Children's Services Singleton Hospital Swansea, UK

Euan Kevelighan

FRCOG, FAcadMed, DipMed Ed

All Wales Head of School & Associate Dean for Obstetrics and Gynaecology Honorary Associate Professor, Swansea University Medical School Honorary Secretary of Welsh Obstetrics and Gynaecology Society Swansea, UK

This edition first published 2018

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Library of Congress Cataloging-in-Publication Data

Names: Webster, Samuel, 1974- editor. | Morris, Geraint, editor. | Kevelighan, Euan, editor.

Title: Essential human development / edited by Samuel Webster, Geraint Morris, Euan Kevelighan.

Description: Hoboken, NJ : John Wiley & Sons, 2018. | Includes index. | Identifiers: LCCN 2017022080 (print) | LCCN 2017037734 (ebook) | ISBN 9781118528600 (pdf) | ISBN 9781118528617 (epub) | ISBN 9781118528624 (pbk.)

Subjects: LCSH: Life cycle, Human. | Developmental biology. | Embryology, Human.

Classification: LCC QP83.8 (ebook) | LCC QP83.8 .E87 2018 (print) | DDC 571.8–dc23

LC record available at https://lccn.loc.gov/2017022080 9781118528624

Cover image: © Nicholas Eveleigh/Gettyimages

Cover design by Wiley

List of Contributors

Rebecca Balfour, MB BCh MRCPCH

Specialty Doctor, Community Child Health

Singleton Hospital

Swansea, UK

Marion Beard, MB BS

Consultant Obstetrician & Gynaecologist

Cardiff and Vale University Health Board

Cardiff, UK

Dana Beasley, State Examination Medicine MRCPCH

Consultant Paediatrician

Morriston Hospital

Swansea, UK

Christopher Bidder, BMedSci BM BS MRCPCH

Consultant Paediatrician with Special Interest in Diabetes and Endocrinology

Morriston Hospital

Swansea, UK

Aisling Carroll-Downey, MB BCh

Belfast City Hospital

Belfast Health and Social Care Trust

Belfast, County Antrim, Northern Ireland

Benjamin Chisholme, MB BCh, BSc (Hons), DRCOG, MRCGP

General Practitioner

Llynfi Surgery

Maesteg

Wales, UK

Jennifer Davies-Oliveira, MB BCh

Speciality Registrar in Obstetrics & Gynaecology

Cardiff and Vale University Health Board

Cardiff , UK

Maitreyee Deshpande, MB BS

Specialty Registrar in Obstetrics & Gynaecology

Cardiff and Vale University Health Board

Cardiff, UK

Jamie Evans, MB BCh MRCPCH

Specialty Registrar, Neonatal Medicine

University Hospital of Wales

Cardiff, Wales, UK

Ruth Frazer, MB BCh

Consultant in Contraception and Sexual Health

Morriston Hospital

Swansea, UK

Nitin Goel, MBBS MD FRCPCH

Consultant Neonatologist

Singleton Hospital

Swansea, UK

Fran Hodge, MB BS

Consultant Obstetrician & Gynaecologist

Morriston Hospital

Swansea, UK

Sharif Ismail, MB BS

Consultant Obstetrician & Gynaecologist

Brighton and Sussex University Hospitals NHS Trust

Sussex, UK

Nisha Kadwadkar, MB BS

Consultant Obstetrician & Gynaecologist

Lancaster Hospital

Lancaster, UK

Euan Kevelighan, FRCOG FAcadMed DipMed Ed

All Wales Head of School & Associate Dean for Obstetrics and Gynaecology

Honorary Associate Professor, Swansea University Medical School

Honorary Secretary of Welsh Obstetrics and Gynaecology Society

Swansea, UK

Aleksandra Komarzyniec-Pyzik, MD Poland, FRSH Dip

Specialty Doctor Obstetrics & Gynaecology

Nevill Hall Hospital

Aneurin Bevan University Health Board

Abergavenny, UK

Franz Majoko, MB BS†

Consultant Obstetrician & Gynaecologist

Formerly of Morriston Hospital

Swansea, UK

Colm McAlinden, MD MB BCh BSc (Hons) MSc, PhD MRCOphth

Visiting Professor

School of Ophthalmology and Optometry

Wenzhou Medical University, China

Geraint Morris, MB BCh FRCPCH

Consultant Neonatologist and Clinical Director, Children's Services

Singleton Hospital

Swansea, UK

Ian Morris, MB BS (Hons) MRCPCH

Consultant Neonatologist

University Hospital of Wales

Cardiff, UK

Marsham Moselhi, MB BS

Consultant Obstetrician & Gynaecologist

Morriston Hospital

Swansea, UK

Deepa Balachandran Nair, MB BS

Registrar in Obstetrics and Gynaecology

Morriston Hospital

Swansea, UK

Manju Nair, MB BS

Consultant Obstetrician & Gynaecologist

Morriston Hospital

Swansea, UK

Cerys Scarr, MB BS

Consultant Obstetrician & Gynaecologist

Royal Gwent Hospital

Newport, UK

Lakshmipriya Selvarajan, MBBS MRCPCH

Specialty Registrar, Paediatric Gastroenterology

Birmingham Children's Hospital

Birmingham, UK

Catrin Simpson, MB BCh BSc (hons) MRCPCH

Consultant Community Paediatrician

Cardiff and Vale University Health Board

Cardiff, UK

Gurpreet Singh Kalra, MB BS

Consultant Gynaecologist

Morriston Hospital

Swansea, UK

Alan Treharne, MB BS

Specialty Registrar, Obstetrics and Gynaecology

St Georges Hospital Medical School

Cardiff, UK

Surekha Tuohy, MB BS MRCPCH

Consultant Community Paediatrician

Singleton Hospital

Swansea, UK

Pramodh Vallabhaneni, MB BS MRCPCH Dip Medical Education

Consultant Paediatrician

Morriston Hospital

Swansea, UK

Sophie Walker MB BS

Clinical Research Fellow

Queen Mary University of London

London, UK

Samuel Webster, PhD FHEA

Senior Lecturer in Anatomy & Embryology

Swansea University Medical School

Swansea, UK

Shabeena Webster, MBBCh MRCPCH Dip Paed Neurodis

Specialty Registrar, Community Paediatrics

Llandough Hospital

Cardiff, UK

Cathy White, MB BS FRCP FRCPCH

Consultant Paediatric Neurologist

Morriston Hospital

Swansea, UK

Bethan Williams, MB BCh MRCPCH

Consultant Community Paediatrician

Cardiff and Vale University Health Board

Cardiff, UK

Toni Williams, MB BCh MRCPCH

Consultant Paediatrician

Glangwili Hospital

Carmarthen, UK

Kinza Younas, MB BS

Consultant Obstetrician & Gynaecologist

Morriston Hospital

Swansea, UK

†Recently deceased.

Preface

Medical education is forever expanding as our understanding of medicine and the human body broadens. Books become larger, thicker and are continually updated. This book combines subject areas associated with biological human development for the undergraduate student new to these fields and for the postgraduate looking for a resource to refer to. Chapter authors and editors have selected topics and focused study upon areas chosen for their importance and likely occurrence. This has created a single resource to help inform the reader and prepare them for clinical work.

The book is organised around the human life cycle, beginning with fertilisation and embryological topics, continuing through obstetric medicine, then neonatal care and child health, and ultimately leading into further fertility and gynaecological medicine.

Each chapter begins with a hypothetical clinical case. Each case relates to important aspect(s) of the chapter, intending that the reader considers the problems posed while reading. Every chapter concludes with more information about the case derived from the results of investigations or treatments, and discusses what has occurred and how the person may be treated, and may also discuss likely effects on that person's future.

Topics within the chapter have been organised into chunks, limiting the size of each section and making searching for information easier and faster. Chapters include key information points that summarise the main ideas discussed, and each chapter has an online collection of single best answer (SBA or multiple choice) and extended matching questions (EMQs) to test the reader's understanding. Some of the questions may extend outside the written chapter.

In this way we have aimed to produce a helpful, informative and more concise resource for a wide range of associated topics. This blending of subjects and disciplines matches many modern medical curricula.

Samuel WebsterGeraint MorrisEuan Kevelighan

How to Use Your Textbook

Features contained within your textbook

Every chapter begins with the learning outcomes to the topic.

Case studies give further insight into real-life patient scenarios.

Key learning points give a summary of the topics covered in a chapter.

Your textbook is full of illustrations and tables.

The website icon indicates that you can find accompanying self-assessment resources on the book's companion website.

About the Companion Website

Don't forget to visit the companion website for this book:

www.wileyessential.com/humandevelopment

There you will find valuable material designed to enhance your learning, including:

Multiple choice questions (MCQs)

Extended matching questions (EMQs)

Part 1Fertilisation

Chapter 1Principles of Development

Sam Webster

Case

Jamie is a 4-month-old boy presenting with disparity between limb length, trunk length and cranial circumference. His height is under the fourth percentile, his weight is under the fourth percentile and his head circumference is above the 97th percentile. Motor development milestones are delayed. Jamie's mother and father have typical heights (168 cm and 176 cm respectively).

Learning Outcomes

You should be able to recognise the stages of cell division in mitosis and meiosis.

You should be able to describe the basic principles of growth and differentiation.

Chromosomes

As a basis of biology cell theory is a crucial part of understanding development. Complex organisms grow from a single cell. The cell is the fundamental unit of structure in the organism, and new cells are formed from existing cells. All structure, function and organisation relates to the unit of the cell. In development we consider how the cells of the gametes merge to form a cell with a new genetic composition, the division of that cell to form new cells, and how those cells become organised, form shapes and tissues of multiple differentiated cell types.

DNA is stored in chromatin form within the nuclei of cells, and RNA is present in the cytoplasm. When cells divide the chromosomes are duplicated and the daughter cells gain exact copies of the DNA of the parent cell (hopefully, if the replication and error checking mechanisms work correctly).

Somatic cells contain 23 pairs of chromosomes including 22 pairs of autosomes and one pair of sex chromosomes (Figure 1.1). Each chromosome is an organised package of DNA.

Figure 1.1Human karyotype. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

In a homologous pair of chromosomes the same genes are encoded on each chromosome but the genes may occur as slightly different versions. One chromosome has been inherited from the father, and the other from the mother. For example, the gene for head hair pigment colour will occur on both chromosomes of a homologous pair, but one copy may encode for blonde hair and the other for brown. These copies are alleles, and the dominant pigment allele will be represented in the phenotype of the individual. This is a simplified example, and many hair pigments are at play in determining a person's final hair colour, accounting for the wide variation of natural shades that occurs. The mixing up of alleles across homologous chromosomes during cell division is an important part of the genetic diversity advantage given by sexual reproduction over asexual reproduction.

If a cell has two copies of each kind of chromosome (e.g. one copy from the mother and one copy from the mother) it is said to be diploid. If it only had one copy it would be haploid.

We can also describe a cell by the number of copies (n) of each unique double-stranded length of chromosomal DNA. Chromosomal DNA inherited from the mother is different to chromosomal DNA inherited from the father. In a pair of chromosomes the genes are the same but the alleles are different. A haploid cell has only one copy of each kind of chromosome so it is described as 1n. Somatic cells are normally diploid, and during part of the cell cycle only have one DNA strand for each kind of chromosome so are described as 2n. They have two copies of each kind of chromosome (one from the mother and one from the father). When a cell copies its DNA in preparation for cell division it will have four copies of each kind of chromosome and be described as 4n.

If the DNA strand of a chromosome is duplicated its two duplicates are joined together at the centromere forming the familiar X shape of most chromosomes (Figure 1.2). Each of the two duplicates is a sister chromatid.

Figure 1.2The structure of a chromosome. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

Mitosis

Mitosis is the process by which cells divide and increase in number in eukaryotic organisms. The result of mitosis is two daughter cells that contain the same genetic information. Mitosis is the method by which cells repair tissues, it is one way in which growth can occur, and it is how cells lost through normal processes are replaced. Some cells are very good at proliferating by mitosis, such as epidermal keratinocytes, which are lost daily as flakes of skin, and some cells are very poor at mitotic division, such as neurones of the central nervous system, which are expected to survive for the lifetime of the organism (although it is not yet clearly understood how long neurones live, but they are not naturally replaced after brain damage). Mitosis is a major mechanism of growth in the embryo and fetus.

Cell division is a step within the cell cycle (Figure 1.3). The cell cycle describes a series of carefully controlled events in the life of cell that take part in cell division, and cells that do not divide are considered to have left the cell cycle. The stages of the cell cycle are gap 1 (G1), synthesis (S), gap 2 (G2) and mitosis (M). The stages of G1, S and G2 are also known collectively as interphase. A cell's DNA is duplicated during S phase, adding a sister chromatid to the existing chromatid. A cell that no longer divides can be described as existing within a G0 phase.

Figure 1.3The cell cycle. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

When a cell begins mitosis its chromosomes become condensed and form their recognisable X shapes during the first phase of mitosis, called prophase (Figure 1.4). At this stage it is diploid (4n). Centrioles are cylindrical structures that have a number of functions within eukaryotic cells, and during mitosis they arrange and separate DNA. During prophase the centrioles move to opposite ends of the cell.

Figure 1.4Mitosis. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

In the next stage, prometaphase, the nuclear membrane breaks down and disappears releasing the DNA into the cytoplasm. Microtubules link the centromeres of the chromosomes to the centrioles, and during metaphase the chromosomes begin to move, pulled by the microtubules to line up along the middle of the cell.

The centromeres are cut in the telophase step, splitting each chromosome into its separate, genetically identical chromatids. One of each pair of chromatids is pulled to opposite ends of the cell by microtubules and the centrioles.

In telophase the chromatids reach the ends of the cell, begin to lengthen again and are no longer visible under a light microscope. Two new nuclear membranes begin to form around the chromatid DNA to create two nuclei. Cytokinesis follows during which a ring of actin filaments appears around the midline of the cell and shrinks, splitting the cell into two. Mitosis is complete, and the two cells return to the G1 phase. During the G1 phase each cell has a full, diploid complement of DNA but only one copy of each chromosome (2n).

Meiosis

Meiosis is a specialised method of cell division in eukaryotes that produces gamete cells. The primary function of meiosis is to produce cells with a haploid (n) complement of chromosomes. Somatic cells have two homologous copies of each chromosome (diploid) and gametes have one copy of each chromosome (haploid, n). When the male and female gametes combine during fertilisation the resulting cell has a restored, diploid complement of 23 pairs of chromosomes.

Meiosis is similar to mitosis, but differs in a couple of ways. Cell division occurs twice during a full cycle of meiosis, producing four daughter cells from one cell. Alleles of homologous chromosomes are randomly exchanged between those chromosomes during a process known as homologous recombination. Cells produced as a result of meiosis will have all of the genes of the parent cells (hopefully in the same locations within chromosomes as the parent cells if the process occurs accurately) but with a random allocation of the alleles of those genes. This genetic variability is an important advantage of sexual reproduction over asexual reproduction. If, for example, the original diploid cell contained the allele for a blue iris on one chromosome and the allele for a green iris on the homologous chromosome, any cell formed as a result of meiosis could contain either allele. Alleles of the genes on the same chromosome may or may not be carried across with the allele for iris colour, as homologous recombination maintains the order of genes but alleles may be swapped around.

During S phase the cell's DNA is duplicated. The two parts of meiosis are described as meiosis I and meiosis II. Prophase I begins with homologous recombination of DNA across homologous chromosomes before the chromosomes shorten, thicken and become condensed (Figure 1.5). The centrioles move to either end of the cell and microtubules are extended, beginning to form the mitotic spindle. The cell at this stage has a diploid (4n) complement of DNA. Metaphase I follows, with the chromosomes aligning themselves along the midline of the cell. During anaphase I pairs of homologous chromosomes split up, with one chromosome of each pair pulled to either end of the cell by the mitotic spindle. Each chromosome at this stage is made up of a pair of identical sister chromatids joined together at the centromere. With telophase I , two new nuclear membranes form around the chromosomes that have collected at either end of the cell, forming two nuclei. An actin ring appears around the middle of the cell and constricts, splitting the cell into two daughter cells by cytokinesis. The cells resulting from meiosis I are haploid (2n). They have 23 chromosomes and each chromosome has two chromatids. The chromosomes are not paired at this stage.

Figure 1.5Meiosis. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

In the second part of meiosis the cell goes through division again, beginning with prophase II. The cell's DNA is not duplicated between meiosis I and meiosis II, so it enters the second part with the haploid (2n) complement of chromosomes. Again the chromosomes are in a condensed, thickened configuration and the centrioles move to either end of the cell. In prometaphase II the nuclear membranes break down and microtubules link the chromosomes to the centrioles. The chromosomes become aligned along the middle of the cell during metaphase II, and then the chromosomes are split during anaphase II. The chromosomes are divided into their two sister chromatids, which are each pulled towards opposite ends of the cell. In telophase II the chromatids reach the ends of the cell and nuclear membranes begin to form around them, forming two nuclei. Cytokinesis forms an actin ring around the middle of the cell that contracts and splits the cell into two.

At the end of meiosis four cells have been produced from one, and each cell has 23 unpaired chromosomes. Each cell is haploid (n).

Spermatogenesis

Spermatogenesis describes the development of haploid spermatozoa from germ cells in the testes. The germ cells of the seminiferous tubules are diploid spermatogonia (typically 2n before they duplicate their DNA to 4n for cell division) with a full complement of chromosomes, including X and Y sex chromosomes. Spermatogonia maintain their numbers throughout life by mitotic division.

Spermatogenesis comprises two stages: spermatocytogenesis and spermiogenesis. A type A spermatogonium cell from the pool of proliferating cells will enter the process of maturation, becoming a type B spermatogonium B cell (Figure 1.6). Groups of type B spermatogonia cells begin spermatocytogenesis in synchrony, eventually producing large numbers of mature spermatozoa. Type B spermatogonia cells are linked to one another at this stage by cytoplasmic bridges and divide mitotically, increasing their numbers and becoming primary spermatocytes.

Figure 1.6Spermatogenesis. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

Primary spermatocytes enter the first round of meiotic division (meiosis I). One diploid (4n) primary spermatocyte becomes two haploid (2n) secondary spermatocytes, and a secondary spermatocyte may contain either an X or a Y sex chromosome as part of their complement of 23 chromosomes. During this first round of meiosis homologous recombination of chromosomes occurs.

Secondary spermatocytes divide again through the stages of meiosis II. The resulting cells are spermatids (haploid, n) and four spermatids are derived from one primary spermatocyte. There are 23 unpaired chromosomes within each cell at the end of meiosis II. The spermatid stage marks the end of spermatocytogenesis.

Clinical Notes 1.1 Male Fertility

Biological and environmental factors can affect the processes of spermatogenesis, producing abnormal sperm. These factors include smoking, sexually transmitted diseases, toxins, increased testicular temperature and radiation. During semen analysis the spermatozoa are graded by counting the total number of spermatozoa and their concentration, the proportions of motile cells and live cells, and the proportion of abnormal sperm cells. Volume, pH and liquefaction time may also be measured.

The spermatid changes shape, lengthening and forming a rounded head and an elongated tail during the process of spermiogenesis. The tail is packed with mitochondria, the cell loses cytoplasm, and the head contains the nucleus. An acrosome layer of specialised enzymes that will enable penetration of an ovum forms around the head of the cell. With these changes the spermatid becomes a spermatozoon.

These processes of spermatogenesis take around 64 days to produce spermatozoa from spermatogonia A cells, and the spermatozoa remain inactive as they are passed to the epididymis. They continue to mature over a seven-day period within the epididymis, at which point they become motile and ready for fertilisation.

Oogenesis

Oogenesis describes the development of haploid oocytes, within follicles, from germ cells in the ovaries. Female germ cells are diploid and contain a pair of X sex chromosomes. They divide mitotically to produce a large number of oogonia, which will enter meiosis (Figure 1.7).

Figure 1.7Oogenesis. (Source: S. Webster and R. de Wreede (2016) Embryology at a Glance, 2nd edn. Reproduced with permission of John Wiley & Sons, Ltd.)

Oogonia begin meiosis I during the 12th week of fetal development. The cell at this stage is known as the primary oocyte, and becomes surrounded by a thin layer of squamous epithelial cells to form a primordial follicle. The primary oocyte only passes through meiosis as far as prophase I with homologous recombination and condensation of the chromosomes (diploid, 4n). The primary oocyte is held, paused in this state. It will only continue its development if it is released from the ovary by ovulation.

Millions of primordial follicles are formed during the first trimester but many degenerate leaving around 400 000 follicles at birth. When puberty begins some of the paused primary oocytes continue their development. Each month a few primordial follicles change. The primary oocyte within becomes larger and the follicular cells become cuboidal. The follicular layer thickens to form a primary follicle. The follicle becomes a secondary follicle when more than one layer of follicle cells has developed. The granulosa cells of the follicle and the oocyte create a layer of glycoproteins on the surface of the oocyte. This layer is the zona pellucida and has important functions during fertilisation (see also Chapter 4).

Although during any particular monthly cycle a number of follicles begin to develop further only one continues leaving the others to degenerate. It is not clear how one follicle is chosen over the others. In the follicle that survives the number of layers of follicular cells continues to increase, and the follicle becomes an antral follicle when it has more than five layers of cells. An antrum appears as a space between the layers of granulosa cells, and this structure becomes the cumulus oophorus.

The follicle is embedded within an ovary, and has been growing and becoming a more prominent structure. The cells of the ovary around the follicle now respond to the follicle's development by differentiating to build two layers of theca interna and theca externa. The follicle is considered to be a mature vesicular follicle (or Graafian follicle). In response to luteinising hormone (LH), thecal cells produce androgens, which are converted into oestrogen. Oestrogens cause repair and thickening of the endometrial lining of the uterus between days 5 and 14 of the menstrual cycle, preparing the endometrium to receive a blastocyst (see Chapter 4).

Only now, in response to spikes in LH and follicle-stimulating hormone (FSH), does the oocyte resume meiosis I and continue in its stalled processes of cell division. At the end of meiosis I the cell divides into a large secondary oocyte (haploid, 2n) and a small polar body (haploid, 2n). The oocyte retains most of its mass and cellular components and the polar body acts as a vessel for the removed chromosomal material. The oocyte is now a haploid cell and the polar body degenerates.

The secondary oocyte enters meiosis II but stalls again, during metaphase II. It will only continue to divide if it is fertilised by a spermatozoon. If this occurs the cell becomes the definitive oocyte (haploid, n, if considered on its own and ignoring the spermatozoon) and produces a second polar body (haploid, n)

If you do the maths and assume that ovulation begins with puberty at around age 11, and ends with menopause at around age 55, at 12 ovulations per year for 44 years only 528 primary oocytes (in this scenario) will continue their development. In truth, only if an oocyte is fertilised by a spermatozoon will it complete meiosis (see Chapter 4), so of the millions of oogonia originally produced only a few are likely to survive.

Clinical Notes 1.2 Female Fertility

The arrested development of the primary oocyte in ­meiosis I may last for 40 or 50 years. Some oocytes will not be stimulated to continue until a menstrual cycle late in reproductive life. The likelihood of DNA fragmentation of a cell increases with time, and DNA fragmentation within these oocytes is more common in older women. This may be the reason for reduced fertility with increasing age.

Growth

Biological growth may be defined as an increase in the mass or size of a tissue or organism, and is a key process of development. Growth can occur through three mechanisms: an increase in cell number, an increase in cell size, or an increase in extracellular material.

Cellular proliferation, that is, an increase in cell number through mitotic cell division, is the most common method of achieving growth. The cells of many adult tissues are also able to proliferate, often as part of a repair mechanism in response to injury. Some adult tissues are very good at cellular proliferation, and some are very poor. Stem cells are an important source of cell renewal in tissues that lose cells constantly, such as the epidermis of the skin and the epithelium of the gut.

Cellular hypertrophy describes an increase in cell size, and is a normal part of the endochondral ossification process, for example, in which chondrocytes lay down a cartilaginous precursor that is modified by hypertrophic chondrocytes and replaced by bone. In adult tissues skeletal muscle responds to the repeated loading of weight training with hypertrophy.

Cells of connective tissues secrete and surround themselves with the extracellular matrix that forms much of the tissue. Chondrocytes and osteocytes increase the amount of matrix in response to loading, increasing the size of the tissue by accretion.

Differentiation

Embryological multipotent cells have the potential to form the wide range of cells needed to build the structures and tissues of the embryo. The process of an embryonic stem cell becoming a specialised, determined, mature cell type is differentiation. The differentiated cell type is stable, meaning that cells formed as a result of mitotic division are typically of the same cell type. Differentiated cells do not normally change cell type, but it is possible to take some mature cells and direct them to dedifferentiate and return to a stem-cell-like state in the laboratory. Adult stem cells also exist and are partly differentiated and able to produce a limited number of cell types, often relevant to the tissue in which they reside.

Signalling

A signal produced by a cell or group of cells is able to influence another cell or group of cells that have receptors for that signal. This is an important concept in embryological development, and much of contemporary research investigates what signals are involved and how they affect cells during development.

Hormones are an example of a signal in adult physiology, and often act in a system-wide manner by passing through the circulatory system from a local source to cells elsewhere in the body. In the embryo the signals may remain attached to the secretory cell or be released to diffuse through the tissue. The distances involved are very small.

Cells respond to the signals in different ways, by differentiating, migrating, proliferating, changing shape, or entering apoptosis, for example.

Organisation

The first shape that the embryo forms after the embryoblast ball of cells is a flat sheet. The sheet appears to be a uniform, oval plate of cells, and to the eye it would be difficult to guess which end will be the head or the tail, and which side is left and right, yet the cells by this point are organised and will respond to one another to form the structures, cell types, and tissues appropriate to the region they are within and the phase of development.

Cells are aware of their location within the embryo. One way in which this can occur is by the diffusion of signalling molecules synthesised by one group of cells across the tissue, and a variable response to the concentration of that signal by cells with appropriate receptors. The cells may respond differently depending upon whether the concentration of the molecule is high, low or somewhere in between.

Morphogens acting as signals in this way are a fundamental part of development. If this signalling is interfered with it can have profound effects and may prevent the embryo from continuing to develop or cause a congenital abnormality.

Morphogenesis

The formation of shape during development is morphogenesis. Cells are able to change their shape, extend processes to pull themselves along and migrate, and a tissue may grow in size. These are all processes that occur during development to cause cells to form shapes and structures. The flat sheets of the germ layers roll up in the very early stages of development, forming tubes and spaces, for example.

Summary

Clinical Case

Investigations and Treatments

Jamie is displaying characteristic features of achondroplasia. He has disproportionate short stature, macrocephaly (large cranium), megaloencephaly (large brain), frontal bossing (a prominent forehead), a low nasal bridge, and some facial features are underdeveloped. Jamie has a long trunk and shortened limbs. He has limited elbow extension and forearm supination.

The diagnosis can be further confirmed by radiology and genetic analysis. Radiological investigations will give further insight into specific aspects of Jamie's condition. Jamie will have hypermobile joints and display genu varum (bowed legs). His hearing should be assessed regularly as children with achondroplasia are more likely to develop middle ear infections. Children with achondroplasia are also more likely to have obstructive sleep apnoea.

Case Conclusions

There is no cure for achondroplasia, and Jamie may develop a number of issues as he grows. It is typically caused by a mutation in the FGFR3 gene that encodes a fibroblast growth factor receptor important in bone and brain growth and development. The mutation is inherited in an autosomal dominant pattern, and only one copy of the defective gene will cause achondroplasia. If two copies of the gene are inherited the developmental defects are likely to be severe enough to cause death, as the thoracic cage is too poorly developed for effective respiration.

In most cases of achondroplasia both parents are of normal height and are not carriers of a defective FGFR3 gene. The cause of achondroplasia in these cases is a spontaneous mutation of the gene.

It is likely that Jamie will develop normal intelligence although developmental milestones will be delayed. Milestones and growth charts for children with achondroplasia can be used to track Jamie's development and growth. He should have a normal lifespan and live independently when he becomes an adult. He may develop spinal and joint problems, or respiratory and cardiovascular difficulties during his development or later in life.

Key Learning Points

An understanding of spermatogenesis and oogenesis helps explain many causes of subfertility.

Men are able to produce new gametes throughout life, but a woman's ova are all produced before birth and are suspended partway through meiosis until each is selected during an ovulatory cycle. The decision to have children later in life has effects on fertility and on the risk of occurrence of some congenital genetic conditions.

The processes of growth are relevant to embryonic development, fetal growth, childhood development and adolescence. In adults processes of repair are similar.

Now visit www.wileyessential.com/humandevelopment to test yourself on this chapter.

Chapter 2The Female Reproductive System

Sam Webster

Case

A 39-year-old woman and her 36-year-old husband present to you in your primary care clinic describing their inability to conceive despite regular, unprotected intercourse for 2 years. You find out that Mrs Amble has a regular 28-day menstrual cycle, that she has never been pregnant, they both have a good understanding of the timings of ovulation and the fertility period, neither smoke nor take recreational drugs, and both drink alcohol occasionally in moderation. Mrs Amble is of normal weight for height and her blood pressure is within the normal range. Mr Amble has never had abdominal or pelvic surgery. She had her appendix removed when she was 15 years old. Neither have a history of urinary tract infections or any sexually transmitted disease, nor diabetes mellitus or thyroid problems. The husband had mumps as a child, and has worked as an electrical engineer for 15 years. Mrs Amble works as a school teacher.

Learning Outcomes

You should be able to recognise the anatomical structures of the female reproductive system and pelvis.

You should be able to describe the physiology of the menstrual cycle.

Anatomy

Bones of the Pelvis

The pelvis forms initially as three separate bones on either side, joined by cartilage. The three bones are the ilium, the ischium and the pubis (Figure 2.1