medicine

2. Mind Maps
for Medical
Students
Clinical Specialties
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3. K30033_C000.indd 2 28/02/17 2:09 pm

4. iii
Olivia Smith
BSc (Hons), MSc (Dist)
Mind Maps
for Medical
Students
Clinical Specialties
The HullYork Medical School
Hull andYork, UK
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5. CRC Press
Taylor & Francis Group
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© 2017 by Taylor & Francis Group, LLC
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Printed on acid-free paper
International Standard Book Number-13: 978-1-4987-8219-7 (Paperback)
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all reasonable efforts have been made to publish reliable data and information, n either the
author[s] nor the publisher can accept any legal responsibility or liability for any errors or
omissions that may be made. The publishers wish to make clear that any views or opinions
expressed in this book by individual editors, authors or contributors are personal to them and
do not necessarily reflect the views/opinions of the publishers. The information or guidance
contained in this book is intended for use by medical, scientific or health-care professionals and
is provided strictly as a supplement to the medical or other professional’s own judgement, their
knowledge of the p atient’s medical history, r elevant manufacturer’s instructions and the
appropriate best practice guidelines. Because of the rapid advances in medical science, any
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The reader is strongly urged to consult the relevant national drug formulary and the drug
companies’ and device or material manufacturers’ printed instructions, and their websites,
before administering or utilizing any of the drugs, devices or materials mentioned in this book.
This book does not indicate whether a particular treatment is appropriate or suitable for a
particular individual. Ultimately it is the sole responsibility of the medical professional to make
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6. v
Dedication vi
Foreword vii
Preface viii
Abbreviations ix
Chapter 1 Psychiatry1
Chapter 2 Obstetrics33
Chapter 3 Gynaecology71
Chapter 4 Paediatrics103
Chapter 5 Ophthalmology157
Chapter 6 Ear, nose and throat 171
Chapter 7 Dermatology183
Chapter 8 Orthopaedics219
Appendix 1 Useful diagnostic classifications 253
Appendix 2 Useful websites 254
Index 257
Contents
Please note due to the layout of the maps and tables, some pages within chapters
have been left intentionally blank
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7. vi
For my father and mother.
This book is dedicated to my parents who have been the greatest influence in my life.
For all your unceasing encouragement, love and support I am forever grateful.
Dedication
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8. vii
Medical students and trainees are faced with a huge volume of facts and knowledge
that they must learn, assimilate and understand how to apply. Many hours are spent
pouring over text books, online resources, lecture notes and papers. This tsunami of
information is often hard to make sense of and the essentials difficult to remember.
Mind maps have become a popular way to help people understand complex
interconnected concepts and information. Diagrams are used to visually organise
information and show relationships among pieces of the whole. Despite technological
advances, when it comes to efficient learning, simple methods, such as that used by
Olivia Smith in Mind Maps for Medical Students: Clinical Specialities, can be highly
effective.
Mind maps can take a lot of time to create. In this compact volume Olivia Smith,
a senior medical student, has helped to do this for readers across eight core clinical
specialities essential to the study of medicine. This is a sequel to her successful first
book, Mind Maps for Medical Students, which distills a wide range of knowledge
according to body systems. Both books organize a large amount of material in a logical,
concise and conceptually appealing way to aid learning. By doing so it complements,
but does not replace, more exhaustive sources and will also allow readers to position
and contextualize new evidence as it emerges, so adding to their knowledge base.
It can be used by medical students,junior doctors and other health care professionals
as a brief overview to introduce an area, for intense periods of revision and as an aide-
mémoire. I hope this will encourage learners to develop their own mind maps in these
or other areas and inspire other medical students to write.
Professor Trevor A Sheldon DSc, FMedSci
Dean, Hull York Medical School, UK
Foreword
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9. viii
This book serves as a companion to Mind Maps for Medical Students. It aims to cover
succinctly the main topics in clinical specialties that students and junior doctors are
expected to be familiar with. It is a distillation of knowledge that aims to complement
larger texts rather than replace them by presenting key facts in a digestible format.Each
topic is presented in a logical manner following a design that may be utilized in OSCE
assessments covering definitions, causes and investigations as well as treatments and
complications.This will aid readers with their revision and consolidation of knowledge
prior to examinations.
Wishing you all the very best in your examinations and future careers.
Olivia Smith BSc (Hons), MSc (Dist)
Final year medical student,The Hull York Medical School, UK.
Preface
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10. ix
Abbreviations
ACE angiotensin converting
enzyme
ACE-III Addenbrooke’s Cognitive
Examination
ACL anterior cruciate ligament
ADHD attention deficit hyperactivity
disorder
ADLs activities of daily living
AIDS acquired immunodeficiency
syndrome
ALL acute lymphoblastic leukaemia
ALT alanine aminotransferase
ANCA antineutrophil cytoplasmic
antibody
AP anteroposterior
APP amyloid precursor protein
ARPKD autosomal recessive polycystic
kidney disease
ASD atrial septal defect
ASO antistreptolysin O
AST aspartate aminotransferase
BBPV benign paroxysmal positional
vertigo
BMI body mass index
BP blood pressure
BUN blood urea nitrogen
CADASIL cerebral autosomal
dominant arteriopathy with
subcortical infarcts and
leukoencephalopathy
CBT cognitive behavioural therapy
CF cystic fibrosis
CFTR cystic fibrosis transmembrane
conductance regulator
CJD Creutzfeldt–Jakob disease
CMV cytomegalovirus
COCP combined oral contraceptive
pill
COPD chronic obstructive pulmonary
disease
CRP C-reactive protein
CT computed tomography
CTG cardiotocography
DDH developmental dysplasia of
the hip
DIC disseminated intravascular
coagulation
DKA diabetic ketoacidosis
DLQI Dermatology Life Quality
Index
DM diabetes mellitus
DMARD disease modifying
antirheumatic drug
DSM-5 Diagnostic and Statistical
Manual of Mental Disorders,
5th Edition
DVT deep venous thrombosis
ECG electrocardiogram/
electrocardiography
ECHO echocardiogram
ECT electroconvulsive therapy
EEG electroencephalogram
ELISA enzyme linked
immunosorbent assay
EPSE extrapyramidal side effects
ESR erythrocyte sedimentation
rate
FBC full blood count
FEV1
/FVC forced expiratory volume in
1 second/fixed vital capacity
FGFR3 fibroblast growth factor
receptor 3
FIGO Fédération Internationale de
Gynécologie et d’Obstétrique
FSH follicle-stimulating hormone
GABA gamma-aminobutyric acid
GAD-7 Generalized Anxiety Disorder
(Assessment)
GFR glomerular filtration rate
GGT gamma glutamyltransferase
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11. x
GI gastrointestinal
GnRH gonadotropin releasing
hormone
HAART highly active anti-retroviral
therapy
HADS Hospital Anxiety and
Depression Scale
hCG human chorionic gonadotropin
HELLP haemolysis, elevated liver
enzymes, low platelet count
(syndrome)
HHV human herpesvirus
HIV human immunodeficiency virus
HPA hypothalamic–pituitary–
adrenal (axis)
HPV human papillomavirus
HRT hormone replacement therapy
HSP Henoch–Schönlein purpura
HSV herpes simplex virus
5-HT 5-hydroxytryptamine
(receptors)
HUS haemolytic uraemic syndrome
IBD inflammatory bowel disease
ICD-10 International Statistical
Classification of Diseases and
Related Health Problems, 10th
Revision
IL interleukin
IM intramuscular
IOP intraocular pressure
IUD intrauterine device
IUGR intrauterine growth
restriction
IUS intrauterine system
IV intravenous
IVF in-vitro fertilization
LABA long-acting beta agonist
LCHAD long-chain 3-hydroxyl-
coenzyme A dehydrogenase
LDH lactase dehydrogenase
LFTs liver function tests
LH leutinizing hormone
LP lumbar puncture
MAO-B monoamine oxidase type B
(inhibitor)
MAOI monoamine oxidase inhibitor
MCV mean corpuscular volume
MMR measles, mumps, rubella
MND motor neurone disease
MRI magnetic resonance imaging
NAAT nucleic acid amplification test
NEC necrotizing enterocolitis
NICE National Institute for Health
and Care Excellence
NICU Neonatal Intensive Care Unit
NMS neuroleptic malignant
syndrome
NNRTI non-nucleoside reverse
transcriptase inhibitors
NRI noradrenaline reuptake
inhibitor
NSAID non-steroidal anti-
inflammatory drug
NTD neural tube defect
OA osteoarthritis
OCD obsessive compulsive disorder
PAS pulmonary artery stenosis
PASI Psoriasis Area and Severity
Index
PCL posterior cruciate ligament
PCOS polycystic ovary syndrome
PCR polymerase chain reaction
PDA patent ductus arteriosus
PEFR peak expiratory flow rate
PET positron emission tomography
PHQ-9 Patient Health Questionnaire
PID pelvic inflammatory disease
POP progesterone only pill
Abbreviations
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12. xi
PPH post-partum haemorrhage
PTSD post-traumatic stress
disorder
PUVA psoralen + ultraviolet
(A spectrum) light
RA rheumatoid arthritis
RAST radioallergosorbent test
RBC red blood cell
RIMA reversible inhibitor of
monoamine oxidase A
RMI Risk of Malignancy Index
RUQ right upper quadrant
SABA short-acting beta agonist
SFH symphysis–fundal height
SHBG sex hormone binding globulin
SJS Stevens–Johnson syndrome
SNRI serotonin noradrenaline
re-uptake inhibitor
SPECT single-photon emission
computed tomography
SSRI selective serotonin re-uptake
inhibitor
STI sexually transmitted infection
SUDEP sudden unexplained death in
epilepsy
SUFE slipped upper femoral
epiphysis
TB tuberculosis
TCA tricyclic antidepressant
TEN toxic epidermal necrolysis
TNM tumour/nodes/metastases
(staging system)
TFTs thyroid function tests
TOP termination of pregnancy
TSH thyroid stimulating hormone
UE urine and electrolytes
uE3 oestriol
UMN upper motor neuron
USS ultrasound scan
UTI urinary tract infection
VDRL Venereal Disease Research
Laboratory (test)
VEGF vascular endothelial growth
factor
VMA/ (urinary) vanillyl mandellic
pHVA acid/plasma homovanillic acid
VSD ventricular septal defect
VZV varicella zoster virus
WCC white cell count
WHO World Health Organization
Abbreviations
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13. K30033_C000.indd 12 28/02/17 2:09 pm

14. MAP1.1 Depression2
TABLE1.1 Treatmentofdepression4
TABLE1.2 Antidepressants6
MAP1.2 Anxiety8
MAP1.3 Obsessivecompulsive­disorder (OCD)10
TABLE1.3 Anxiolyticsandhypnotics12
MAP1.4 Schizophrenia14
TABLE1.4 Antipsychotics16
MAP1.5 Bipolardisorder18
TABLE1.5 Personalitydisorders20
MAP1.6 Anorexianervosa22
MAP1.7 Bulimianervosa 24
MAP1.8 Attentiondeficithyperactivity
­disorder (ADHD) 26
TABLE1.6 Dementia28
ChapterOnePsychiatry
Psychiatry1
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15. Psychiatry2Map1.1.Depression
Treatment
Dependsontheclassificationofdepression.
Itincludespsychologicaltherapiessuchas
CBT,antidepressantsandECT(seeTable
1.1,p.4)
Investigations
Ensurethatthepatientisreallysufferingfromdepressionandnotan
organicdisorder.Thisinvolvestakingacarefulhistoryfromthepatient
andtheuseofquestionnairessuchasHADS,PHQ-9,GAD-7followedby
investigationsdependingonpatientpresentation.
Alwaysassesssuiciderisk.
•Baselinebloods:FBC,UE,LFTs(includingGGTandMCVfor
alcoholmisuse),TFTs(hypothyroidismmaycauselowmood),ESR,
glucose,calcium,vitaminB12andfolatelevels.
•Specifictestsareonlyusedifindicatedbyhistoryandexamination
(e.g.urinefortoxicology,dexamethasonesuppressiontest,syphilis
serologyetc).
•Radiology:CTorMRImaybeindicatedinsomecases.
Causes
Thecauseisacomplicatedinteractionbetweengenetics,neurohormo-
nalandpsychosocialfactors.Afewexamplesaregivenbelow:
•Genetic:familyhistoryofdepression.
•Neurohormonal:themonoaminehypothesisofdepressionispopular,
whichsuggeststhattherearelowlevelsofserotonin,noradrenaline
anddopamineinthebrain.Othertheoriesincludethesuggestionof
increasedcortisollevels.
•Psychosocial:adverselifeeventsandnegativechildhoodexperiences
suchasabuse,thelossofaparentandbullying.Chronicphysical
illness,unemploymentandthelackofaconfidingrelationshipare
linkedtoincreasedratesofdepression.
Whatisdepression?
Thisisaconditionofpervasivelowmood.ItisdiagnosedusingtheICD-
10ortheDSM-5andthefollowingcriterianeedtobefulfilled:
1.Symptomsmustbepresentforatleast2weekswithachangefrom
normalmoodandatleasttwotothreecoresymptoms.
2.Changeinmoodmustnotbesecondarytodrugoralcoholmisuse,a
medicalconditionoranadverselifeeventsuchasbereavement.
3.Theremustbeimpairmentofsocialfunctioning.
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16. Psychiatry3Map1.1.Depression
Classification
Mild(4–5symptoms)
Moderate(6–7symptoms)
Severe(8–10symptoms)Unabletocompletedailytasks
Realdifficultyincompletingdailytasks
Cancontinuewithdailytasks+/–somaticsymptoms
+/–somaticsymptoms
+/–psychoticsymptoms
PresentationSomaticorpsychoticsymptoms
Symptoms
Thesemaybesplitintothreebroadcategories:coresymptoms,negativethinkingandsomaticsymptoms:
Coresymptoms:depressedmood,anergia,anhedonia.
Negativethinking:thoughtsofguilt,lowselfesteem,thoughtsofsuicideanddeath,poorconcentration.
Somaticsymptoms:decreasedweight(increasedweightseeninatypicaldepression),sleepdisturbancewithearlymorningwaking,
decreasedlibido,constipation,psychomotorretardationoragitation.
Thesesymptomsmaybeusedtoclassifydepressionasmild,moderateorsevere:
Psychoticsymptomsaremoodcongruentorincongruent:
Moodcongruent:
•Delusions:ofpoverty,guilt,punishment;ifthepatientholdsthedelusionthattheyaredead,thenthisisknownasCotard’ssyndrome.
•Hallucinations:
Auditory:usuallyderogatoryvoices.
Olfactory:rottingfruit/flesh.
Visual:tormentors.
Moodincongruent:thoughtinsertionorwithdrawal.
MAP1.1.Depression
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17. Psychiatry4Table1.1.Treatmentofdepression
TABLE1.1.Treatmentofdepression.Treatmentdependsontheclassificationofdepression.
ClassificationofdepressionMethodoftreatment
MildConservativetherapy
Thisisa‘watchfulwaiting’approachandinvolves:
• Anexerciseregime:thecurrentrecommendationsarethreetimesaweekfor45minuteslasting10–12weeks
• Alcoholandlifestyleadvice
• Sleephygiene
• Guidedselfhelp
Moderate–severeConservativetherapy:
• Anexerciseregimeasabove
• Psychologicaltherapies(e.g.cognitivebehaviouraltherapy[CBT],whichchallengesthepatient’sthoughtsand
feelingsinordertochangethem),counselling,interpersonalpsychotherapy,dynamictherapy
Medicaltherapy:
• Antidepressants(seeTable1.2,p.6).MostpatientsarestartedonanSSRIfirstline
• Ifthisinitialtherapydoesnotwork,patientsmaybeswitchedtoalternativeantidepressants,havetheirtherapy
augmentedwithantipsychoticorantiepilepticmedicationbyaspecialistorbereferredforECT(usually6–12
sessions,twiceweekly).ThepathwayfolloweddependsonNICEandlocalguidance
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18. K30033_C001.indd 5 28/02/17 11:02 am

19. Psychiatry6
TABLE1.2.Antidepressants.
ClassofantidepressantExamplesUsesSideeffects
Selectiveserotoninreuptake
inhibitors(SSRIs)
Citalopram
Sertraline(oftenusedinthosewho
havepreviouslyhadamyocardial
infarction)
Fluoxetine(hasalonghalf-life)
Paroxetine
DOBS:
Depression
OCD
Bulimia
Socialphobias
• GIupset
• Sexualdysfunction
• Hyponatraemiaintheelderly
• Discontinuitysyndrome:shivering,anxiety,headache,
nausea,dizziness
• Serotoninsyndrome:musclerigidity,seizures,
cardiovascularcollapse,hyperthermia.Treatserotonin
syndromewithcyproheptadine(a5-HT2A
receptor
antagonist)
Tricyclicantidepressants
(TCAs)
Amitriptyline
Imipramine
Clomipramine
DOBS:
Depression
OCD(clomipramine)
Bedwetting(imipramine)
Sometimesneuropathic
pain(amitriptyline)
• Linkedtoreceptorblockade:
○○α1
antagonist:posturalhypotension
○○Antimuscarinic:drymouth,urinaryretention,
constipation,blurredvision
○○Antihistaminergic:weightgain,drowsiness
• Toxicity=the3Cs:
Convulsions
Coma
Cardiotoxicity
Serotoninnoradrenaline
reuptakeinhibitors(SNRIs)
Venlafaxine
Duloxetine
Depression
Generalizedanxietydisor-
der(venlafaxine)
Peripheralneuropathy
(duloxetine)
• Increasedbloodpressure
• Nausea
• Sedation
Table1.2.Antidepressants
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20. Psychiatry7Table1.2.Antidepressants
Monoamineoxidase
­inhibitors(MAOIs)
Selegiline
Moclobemide(reversibleinhibitorof
monoamineoxidaseA[RIMA])
HAD:
Hypochondriasis
Anxiety
Depression
SelegilineisaMAO-B
inhibitorthatislicensed
foruseinParkinson’s
disease
• Antimuscarinic:drymouth,urinaryretention,
constipation,blurredvision
• TheCheeseReaction–hypertensivecrisisthatoccurs
withingestionoftyraminecontainingsubstances
(e.g. cheese,pickledherring,soybeanproducts,etc.)
α2
antagonistMirtazapineDepression
PTSD
• Increasedappetiteandweight
• Drymouth
• Sedation
Noradrenalinereuptake
inhibitors(NRIs)
ReboxetineDAP:
Depression
ADHD
Panicdisorder
• Antimuscarinic:drymouth,urinaryretention,
constipation,blurredvision
• Antihistaminergic:weightgain,drowsiness
TetracyclicsMaprotilineDepression• Sedation
• Posturalhypotension
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21. Psychiatry8Map1.2.Anxiety
Whatisanxiety?
Anxietyisanormalemotionthatlikelyhasbeenexperiencedby
mostofusduringourlives.However,whenanxietyissuchthatit
interfereswithdailyfunctioningandperformance,itisconsideredtobe
pathological.ThisrelationshipiscalledYerkes–Dodsonlaw.
Anxietymaybeclassifiedintomanydifferentsubgroups:
Organiccauses:
•Hyperthyroidism.
•Hypoglycaemia.
•Phaeochromocytoma.
•Cerebraltrauma.
•Temporallobeepilepsy.
Psychiatriccauses:
•Anxietydisorders:
Phobicdisorders(e.g.agoraphobia).
Non-situationaldisorders(e.g.generalizedanxiety
disorder[atriadofapprehension,motortensionand
autonomicoveractivity]).
Reactiontostressfulevents(e.g.PTSD).
OCD(seeMap1.3,p.10).
•Secondarytodepressionorpsychosis.
•Secondarytoamedicalcondition.
•Secondarytopsychoativesubstanceabuse(e.g.alcoholintake
orwithdrawal,amphetamines,benzodiazepinewithdrawal).
Symptoms
Thesemaybegeneralizedorparoxysmal.
RememberasPANICS:
P–Palpitations,pinsneedles
A–Abdominaldiscomfort
N–Nauseaandvomiting
I–Intensefearofdying(angoranimus)
C–Chestpain,choking
S–Sweating,swallowingdifficulty(globushystericus),shortnessof
breath
Thesesymptomsmayoccuratdifferenttimesandofvarying
intensitydependingontheunderlyingdisorder(e.g.ifa
patienthadasocialphobia,thenanexcessiveanxious
responsewouldonlyoccuronaspecificsocialsituationsuch
asdeliveringaspeech).
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22. Psychiatry9Map1.2.Anxiety
Treatment
Dependsonthetypeofanxietydisorder
diagnosed,butconsistsofpsychologicaland
pharmacologicaltherapy.
Psychologicaltherapy:
•CBT.
•Behaviouraltherapysuchasgraded
exposure.
•Psychodynamictherapy.
Pharmacologicaltherapy:
•Antidepressants(seeTable1.2,p.6).
•Anxiolytics(seeTable1.3,p.12).
Investigations
Thereisnospecificinvestigationforanxiety
disorders,butitisvitaltoexcludeanorganic
cause.Therefore,performinitialinvestigations:
•Bloods–FBC,UE,TFTs,glucose,calcium
levels.
•ECG.
•Toxicologyreportifindicated.
•UrinaryVMA/pHVAifindicated(for
phaeochromocytoma).
Causes
Thegenetic/biologicalmodel:
•Inheriteddisorder–manypatientshavea
first-degreefamilyrelativewiththedisorder.
•Abnormalreceptorsinthe5-HT,noradrenaline
andGABAsystems.
Thesocial/psychologicalmodel:
•Responsetostressfullifeevents.
•Apsychologicallysusceptiblepatientmay
misinterpretanormalbodystimulus.
MAP1.2.Anxiety
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23. Psychiatry10Map1.3.Obsessivecompulsivedisorder(OCD)
WhatisOCD?
OCDisapsychiatricdisordercharacterizedbyobsessive
thoughts,ruminationsandcompulsiverituals.Itaffects
menandwomenequally.Themeanageofonsetis
20years.
Theconditionisassociatedwithanankastic
personalitydisorder,GillesdelaTourettesyndrome,
depressionand,lesscommonly,schizophreniaandbasal
gangliadisorders.
Treatment
Psychologicaltherapy:
•CBT.
•Responseprevention.
•Thoughtstopping.
•Cognitivemodelling.
Pharmacologicaltherapy:
•Antidepressants(seeTable1.2,p.6),particularly
clomipramine,whichhasstronganti-obsessional
actions
•Anxiolytics(seeTable1.3,p.12).
•Buspironeisusedifmarkedanxietypresent.
Psychosurgical:
•Thisisrareandonlyconsideredforintractablecases.
Examplesincludestereotacticcingulotomyoryttrium
radioactiveimplants.
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24. Psychiatry11Map1.3.Obsessivecompulsivedisorder(OCD)
Investigations
ThereisnospecifictestforOCD.
(SeeMap1.2,p.8,fortestsrequiredtorule
outorganiccausesofanxietyandothertypes
ofanxietydisorder.)
Causes
•Geneticfactors:3–7%ofsufferershave
afirst-degreerelativewiththecondition.
•Dysregulation/hypersensitivityof5-HT
receptors.
•Hyperactiveorbitofrontallobe.
•Basalgangliadysfunction:
Dysfunctionalstriatum.
Smallercaudatenucleus.
Symptoms
Obsessivethoughts,compulsions,impulses,
ruminationsandrituals.
TheICD-10highlightssixfeaturesthat
arehighlysuggestiveofthedisorder:
1.Obsessionsandcompulsionsthathave
beenpresentforatleast2weeks.
2.Theobsessionsandcompulsionsdecrease
thepatient’sfunction.
3.Thepatientisawarethatthesethoughts
aregeneratedfromtheirownmind.
4.Thesethoughtsareunpleasantlyrepetitive.
5.Atleastoneofthesethoughtsisnot
resisted.
6.Thecompulsionsandritualsperformedare
not,inthemselves,pleasurableforthe
patient.
MAP1.3.Obsessivecompulsivedisorder(OCD)
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25. Psychiatry12Table1.3.Anxiolyticsandhypnotics
TABLE1.3.Anxiolyticsandhypnotics.
DrugnameMechanismofactionUsesSideeffects
Buspirone5-HT1A
partialagonistGeneralizedanxietydisorder• Nauseaandvomiting
• Dizziness
• Headache
• Blurredvision
AmobarbitalIncreasestheinhibitoryaction
ofGABAbybindingtothe
barbituratebindingsiteonthe
GABAA
receptor.Increasedinflux
ofCl-
ions
Severeinsomnia• Dependence
• Withdrawalsymptoms
• Daytimesedation
• Cardiorespiratorydepression
• Druginteractionssinceitinducesp450system
ZolpidemBindstothebenzodiazepine
­bindingsiteontheGABAA
receptor
Insomnia• Dependence
• Tolerance
• Sedation
• Drowsiness
• Dizziness
DiazepamIncreasestheinhibitoryaction
ofGABAbybindingtothe
­benzodiazepinebindingsiteonthe
GABAreceptor.Increasedinflux of
Cl-
ions
Anxiety
Insomnia
Statusepilepticus
• Dependence
• Tolerance
• Cardiorespiratorydepression
• Drowsiness
• Sedation
FlumazenilCompetesatthebenzodiazepine
bindingsite.Itisthereforean
antagonisttotheactionsof
­zolpidemanddiazepam
Benzodiazepineoverdose• Palpitations
• Insomnia
• Convulsion
• Anxiety
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26. K30033_C001.indd 13 28/02/17 11:02 am

27. Psychiatry14
Causes
Theexactcauseofschizophreniaisunknown
buttherearemanytheories:
1.Thedopaminehypothesis–dopaminergic
overactivity.
2.Serotonergicoveractivity–duetothe
superiorityofclozapineintreating
treatmentresistantschizophrenia.
3.Genetics–higherincidenceinthosewitha
familyhistory.AssociationwiththeDISC1
gene(DisruptedInSChizophrenia).
4.Drugabuse–particularlycannabisuseatan
earlyage.
5.GroupApersonalitydisorder.
6.Illnessduringpregnancy.
7.Winterbirths.
8.Adverselifeevents.
Whatisschizophrenia?
Thisisachronicpsychiatricdisorderinwhich
thepatientexperiencesdistortedreality.It
affectsmenandwomenequally,althoughthe
formertendtohaveanearlieronset.The
conditionisassociatedwithahighersuicide
ratethanthegeneralpopulation(10–15%).
Symptoms
TheICD-10suggeststhatsymptomsneedtobe
presentforatleast1month.
Thesesymptomsmaybedescribedas
Schneider’sfirstranksymptoms(rememberas
TAP2)or,morebroadly,aspositiveandnegative
symptoms.
Schneider’sfirstranksymptoms:
•T–Thoughtdisorder–thoughtinsertion,
withdrawal,broadcasting.Thismay
interferewithspeech,leadingto
neologisms,thoughtstoppingand
knight’smovethinking.
•A–Auditoryhallucinations–thoughtecho,
runningcommentary.
•P–Passivityphenomenon–beliefthatbody
iscontrolledbyanexternalagency.
•P–delusionalPerceptions–thinkingan
everydayobjecthasaspecificmeaning
forthepatient.
Positivesymptoms:
•Thoughtdisorder–thoughtinsertion,
withdrawal,broadcasting.
•Delusions.
•Ideasofreference.
Map1.4.Schizophrenia
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28. Psychiatry15Map1.4.Schizophrenia
•Hallucinations.
•Passivityphenomena.
Negativesymptoms(ABCP):
•Alogia.
•Anhedonia.
•Avolition.
•Bluntingofaffect.
•Catatonia.
•Povertyofideation.
Investigations
Thereisnospecificinvestigationforschizophre-
nia.Itisaclinicaldiagnosisbutitisvitaltorule
outothercausesofpsychosis,suchasdrug-
inducedpsychosis,andtoperformarisk
assessment.Moreover,baselinebloodsshouldbe
performedaswellasanECGduetothepossible
sideeffectsofantipsychoticmedication.
Treatment
Dependsonwhetheritisanurgentornon-urgentsituation.Followyourlocalguidelines.
Psychologicaltherapy:
•CBT.
•Familyintervention–prognosisisworseinfamilieswithhighexpressedemotion.
•Arttherapy.
•Liaisewithsocialworkerregardinghousingdifficultiesandemployment.
Pharmacologicaltherapy:
•Antipsychotics(seeTable1.4,p.16).
MAP1.4.Schizophrenia
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29. Psychiatry16Table1.4.Antipsychotics
TABLE1.4.Antipsychotics.
ClassificationExamplesMechanismof
action
UsesSideeffects
TypicalHaloperidol
Chlorpromazine
Thioridazine
BlockD2
receptors,
therebyincreasing
concentrationof
cAMP1
Schizophrenia
Psychosis
Mania
Tourette’ssyndrome
Antipsychoticmedicationsblockseveralreceptors,whichresultsinan
arrayofsideeffects:
• D2
receptorsaffectseveralpathways:
○○Tuberoinfundibularpathway:galactorrhoea,amenorrhoea,
hyperprolactinaemia
○○Nigrostriatalpathway:extrapyramidalsideeffects(EPSE).
RememberasTRAP:
T–Tardivedyskinesia
R–Restlesslowerlimbs(akathesia)
A–Acutedystonia
P–Parkinsonisms
○○Mesocorticalpathway:increasesnegativesymptoms(seeMap
1.4,p.14).
○○Mesolimbicpathway:decreasespositivesymptoms(seeMap
1.4,p.14).
• α1
antagonist:posturalhypotension
• Antimuscarinic:drymouth,urinaryretention,constipation,blurred
vision
• Antihistaminergic:weightgain,drowsiness
• Neurolepticmalignantsyndrome(NMS)–thisisalife-threatening
reactionthatmaybecausedbyanadversereactiontoantipsychotic
drugs.SymptomsofNMSinclude:fever,musclerigidity,altered
mentalstatusandautonomicdysfunction
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30. Psychiatry17
AtypicalOlanzapine
Clozapine
Quetiapine
Risperidone
Aripiprazole
BlockD2
receptors
thereby­increasing
­concentrationof
cAMP1
­receptors,
butarealso
­effectivein
­blocking5-HT2
,α1
andH1
receptors
Schizophrenia
Olanzapinemayalso
beusedforanxiety
disorders,OCD,mania,
depressionand
­Tourette’ssyndrome
• Sideeffectsarethesameasthoselistedfortypicalagents;however,
therearefarfewerEPSEandanticholinergicsideeffects,whichis
whyatypicalagentsarepreferredtotheolder,typicalmedications.
• Specificsideeffects:
○○Clozapine(usedintreatmentresistantschizophrenia):
agranulocytosis
○○Olanzapine:weightgain
MoodstabilizerLithiumUnknown.Thought
toactinasimilar
waytoothersingle
chargedcations
byinterfering
withmembrane
iontransport
­mechanisms
Bipolardisorder
Mania
• Common:tremor,diarrhoea,increasedappetite
• Thosethatrequirebloodtestmonitoring:nephrogenicdiabetes
insipidus,hypothyroidism
• Inoverdose:convulsions,coma,death
• Teratogenic:Ebstein’sabnormality
• Specialpoints:narrowtherapeuticindex.Monitorserumlithium
concentration
Table1.4.Antipsychotics
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31. Psychiatry18Map1.5.Bipolardisorder
Whatisbipolardisorder?
Majordepressionalongsideatleastonemanic
(bipolarI)oronehypomanic(bipolarII)episode
characterizesthisdisorder.Patientswill
eventuallysufferfromdepressivesymptoms.In
somewaysthisdisordermaybeviewedasa
cyclicalinterchangingbetweenelevatedandlow
moodwherethepatientisfunctionallynormal
betweenepisodes.
Menandwomenareequallyaffected.
MAP1.5.Bipolardisorder
Causes
Thecauseisacomplicatedinteractionbetween
genetic,neurohormonal,neuroanatomicaland
psychosocialfactors.Afewexamplesaregiven
below:
Genetic:familyhistorybipolardisorder.
Possibleinvolvementofchromosomes6qand
8q21.
Neurohormonal:themonoaminehypothesis.
Neuroanatomical:increasedsizeoflateral
ventricles,abnormalHPAaxis.
Psychosocial:adverselifeeventsandnegative
childhoodexperiencessuchasabuse,PTSD.
Typesofbipolardisorder
TypesKeyfeatures
BipolarI
BipolarII
Rapidcycling
Cyclothymia
•Atleastonemanic
episodelasting1week.
•Usuallycoupledwith
periodsofdepression,
butsomepatientsmay
onlyhavemanicepisodes.
•1episodeofsevere
depression,butonly
coupledwithhypomania.
•4moodswingswithin
ayear.
•Moodswingsthatarenot
assevereasthosein
bipolardisorder.Follows
acyclicpatternthatmay
lastforlongerperiods.
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32. Psychiatry19Map1.5.Bipolardisorder
Treatment
Dependsonwhetheritisanurgentor
non-urgentsituation.Followyourlocal
guidelines.
Psychologicaltherapy:
•CBT.
•Familyfocusedtherapy.
•Liaisewithsocialworkerregardinghousing
difficultiesandemployment.
Pharmacologicaltherapy:
•Antipsychoticsandmoodstabilizers(see
Table1.4,p.16).
•Antiepilepticmedicationsarealsoused
eitherindependentlyorincombinationwith
lithium.
Investigations
•Thereisnospecificinvestigationforbipolar
disorder.Itisaclinicaldiagnosisbutitis
vitaltoruleoutothercausesofpsychosis,
suchasdrug-inducedpsychosis,aswellas
organicmooddisordersandtoperforma
riskassessment.Moreover,baselinebloods
shouldbeperformedaswellasanECGdue
tothepossibleaffectsofantipsychotic
medication.(Note:QTcprolongationmay
occurwithallantipsychotics.)
•Investigationsasfordepression(seeMap
1.1,p.2).
Symptoms
•Thoseofdepression(seeMap1.1,p.2).
•Thoseofmania:thesesymptomsmustbe
presentforatleast1week.Rememberas
DIGFAST:
D–Distractibility
I–Irresponsiblebehaviour(e.g.hedonistic
behaviourwithoutconsideringthe
consequencessuchasborrowingor
spendingvastsumsofmoneyand
havingunprotectedsexualintercourse)
G–Grandiositywithdelusionsof
power/wealth
F–Flightofideas
A–Activityincreases
S–Sleepdecreases
T–Talkativeness
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33. Psychiatry20Table1.5.Personalitydisorders
TABLE1.5.Personalitydisorders.Thesearepervasivedifficultiesinpersonalitythatimpactuponapatient'ssocial
­functioninginadetrimentalway.Theyareincrediblydifficulttotreatandoftenrequireyearsofpsychotherapy.
ClusterGeneralcharacteristicsSpecificsubtypes
AOddeccentricbehaviour
Donotformmeaningfulrelationships
Psychosisisnotpresent
1. Paranoid:
Suspicious
Defencemechanism:projection
2. Schizoid:
Socialwithdrawal/likessocialisolation
3. Schizotypal:
Eccentricbehaviourandbeliefs
‘Magicalthinking’
BTheemotionalcluster
Associatedwithmooddisorders
Associatedwithsubstanceabuse
1. Antisocial:
Affectsmalesmorethanfemales
Criminalbehaviouranddisregardforothermembersofsociety
2. Borderline:
Affectsfemalesmorethanmales
Associatedwithdepression
Associatedwithdeliberateselfharm
Feelingsofemptiness
Unstableinterpersonalrelationships
Blackandwhitethinking
Impulsivebehaviour
Defencemechanism:splitting
3. Histrionic:
Attentionseeking,veryflirtatiousfemale
Sexuallyprovocative
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34. Psychiatry21Table1.5.Personalitydisorders
4. Narcissistic:
Affectsmalesmorethanfemales
Grandiosedelusions
Lackofempathy
Lovesadmirationandloathescriticism
CTheanxiouscluster
Associatedwithanxietydisorders
1. Avoidant:
Verysensitivetorejection
Avoidssocialsituations
2. Anankastic:
AssociatedwithOCD
Perfectionistpersonalities
3. Dependent:
Lowselfesteem
‘Clingy’
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35. Psychiatry22Map1.6.Anorexianervosa
Treatment
Psychoeducationconcerningweightand
nutrition.
Psychologicaltherapy:
•CBT.
•Familyfocusedtherapy.
•Interpersonaltherapy.
•Psychodynamictherapy.
Pharmacologicaltherapy:
•Correctionofelectrolyteimbalance.
•Restorehealthyweight.
•Prescribemealsthatarenutritionally
appropriate.
Urgentsituationsmayrequirerefeeding
undertheMentalHealthAct.
Whatisanorexianervosa?
Thisisaneatingdisorderthatis
characterizedbyICD-10byfourkeypoints:
1.BMI17.5.
2.Self–inducedweightloss.
3.Amorbidfearoffatness.
4.Endocrinedysfunction(e.g.amenorrhoea).
Thisconditionaffectsfemales10–20times
morethanmales.Itisassociatedwithsocial
classesIandIIaswellascertainprofessions
(e.g.modelsanddancers).
Causes
Thecauseisacomplicatedinteraction
betweengenetics,neurohormonaland
psychosocialfactors.Afewexamplesare
givenbelow:
•Genetic:familyhistoryofanorexia
nervosa.
•Neurohormonal:abnormalitiesin
serotoninmetabolism.
•Psychosocial:adverselifeevents,
perfectionistpersonalities,high
achievingfamilies,mediaexpectations
ofthinnessrelatingtotheidealfemale
form.
MAP1.6.Anorexianervosa
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36. Psychiatry23Map1.6.Anorexianervosa
Symptoms
•Excessiveweightloss.
•Weaknessandfatigue.
•Coldperipheries.
•Bradycardia.
•Hypotension.
•Amenorrhoea.
•Thinlanugohairoverfaceandbody.
•Inabilitytoperformsquattest.
•Co-morbiddepression/OCD.
Signs
•Signsofinducedpurging:
Russell’ssign.
Toothenamelthatispitted/eroded.
Enlargedparotidglands.
•Signsofelectrolyteimbalance:
Cardiacarrhythmias.
Complications
•Death.
•Endocrinedysfunction
(e.g.amenorrhoea).
•Metabolicalkalosis–fromexcessive
vomiting.
•Metabolicacidosis–fromlaxative
abuse.
•Cardiaccomplications(e.g.arrhythmias
andQTprolongationthatmayleadto
suddendeath).
•Refeedingsyndrome–resultsin
hypophosphataemia,whichcanleadto
rhabdomyolysis,arrhythmias,respiratory
failure,convulsions,comaanddeath.
•Electrolyteabnormalities–hypokalae-
mia,hyponatraemia,hypoglycaemia,
hypocalcaemia,hypercholesterolaemia.
•Anaemia.
•Proximalmyopathy.
Investigations
Clinicalassessment:overallclinical
assessmentincludingtheuseoftoolssuch
astheSCOFFquestionnaire:
S–HaveyouevermadeyourselfSick
becauseyouareuncomfortablyfull?
C–DoyoufeelthatyouhavelostControl
overhowmuchyoueat?
O–HaveyoulostOnestoneina3month
period?
F–DoyoubelieveyourselftobeFatwhen
otherssayyouarethin?
F–DoesFooddominateyourlife?
•BMI=weight(kg)/height(m)2
.
•Bloods–FBC,UE,LFTs,TFTs,glucose,
calciumlevels.
•ECG.
•Bloodpressure.
•Toxicologyreportifindicated.
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37. Psychiatry24Map1.7.Bulimianervosa
Symptoms
•Rememberthatpatientsmayactuallybe
overweightduetobingeeatingbehaviour.
•Co-morbiddepression/OCD.
Signs
•Signsofinducedpurging:
Russell’ssign.
Toothenamelthatispitted/eroded.
Enlargedparotidglands.
Oesophagealtears.
•Signsofelectrolyteimbalance:
Cardiacarrhythmias.
Hypokalaemiaisassociatedwithvomiting
aswellaslaxativeabuse.
Whatisbulimianervosa?
Thisisaneatingdisorderthatis
characterizedbyICD-10bythreekeypoints:
1.Patientengagesinbingeeating.
2.Thereisevidenceofpurgativebehaviour
(e.g.vomitingtocounteracttheeffectsof
bingeeatingandincreasedweight).
3.Amorbidfearoffatness.
Causes
Thecauseofbulimiaisunclear,butitisthought
tobeduetocomplexinteractionsbetween
genetic,neurohormonalandpsychosocialfactors.
Afewexamplesaregivenbelow.
Genetic:familyhistoryofbulimianervosa.
Neurohormonal:theoriesinvolvingalterationof
serotoninandnoradrenalineexist.
Psychosocial:adverselifeevents,perfectionist
personalities,pastdietingbehaviour,anorexia
nervosa,personalitydisordersparticularly
borderlinepatients,lowselfesteemand
depression.
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38. Psychiatry25Map1.7.Bulimianervosa
Treatment
Psychologicaltherapy:
•CBT.
•Familyfocusedtherapy.
•Interpersonaltherapy.
•Psychodynamictherapy.
Pharmacologicaltherapy:
•Correctionofelectrolyteimbalance.
•AntidepressantssuchasTCAsandSSRIshave
beenshowntodecreasepurgativebehaviour.
Urgentsituationsarelesscommonthanfor
anorexianervosasincepatientsareoftenof
normalweight.
MAP1.7.Bulimianervosa
Investigations
Likeanorexianervosa,thereisnospecific
underlyingtestforbulimianervosa.However,itis
importanttoruleoutorganiccausesofweight
gainandweightlossaswellasperforminga
psychiatricevaluation.Itisimportanttoperform
theinvestigationslistedbelow,particularlyUE,
sinceelectrolytedisturbancesarecommonwith
purgativebehaviour.
•BMI=weight(kg)/height(m)2
.
•Bloods–FBC,UE,LFTs,TFTs,glucose,calcium
levels.
•ECG.
•Bloodpressure.
•Toxicologyreportifindicated.
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39. Psychiatry26Map1.8.Attentiondeficithyperactivedisorder(ADHD)
Complications
•Substancemisuse.
•Dissocialpersonalitydisorder.
•Unemployment.
•Lowselfesteem.
•Increasedrateofsuicide.
WhatisADHD?
Thisispervasive,developmentallyinappropriate
behaviourinwhichthepatientlacksconcentration
andishyperactive.Itismorecommoninmales
thanfemalesandmustbepresentinatleasttwo
differentsettings(e.g.athomeandatschool).The
symptomsmustbepresentforatleast6months.
Causes
Thecauseisacomplicatedinteractionbetween
genetics,neurohormonalandpsychosocialfactors.
Afewexamplesaregivenbelow.
Genetics:possibleinvolvementofchromosomes
5,6and11.
Neurohormonal:dysregulationofdopamineand
noradrenaline.
Psychosocial:familialdysfunction,parental
stress,potentiallyfoodadditives.
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40. Psychiatry27Map1.8.Attentiondeficithyperactivedisorder(ADHD)
Symptoms
•Decreasedconcentration.
•Poorschoolperformance.
•Forgetfulness.
•Hyperactivebehaviour.
•Inabilitytoorganizetasks.
•Fidgeting.
•Verytalkative.
•Ofteninterrupts.
Treatment
Psychologicaltherapy:
•CBT.
•Familyfocusedtherapyincludingparent
managementtherapy.
•Educationalintervention.
Pharmacologicaltherapy:
•Methylphenidate(Ritalin)isthetreatmentof
choice.
Investigations
•ThereisnospecifictestforADHD,butitis
importanttoperformafulldevelopmental,
medicalandfamilialassessmentaswellas
obtaininginformationfromthechild’sschool
concerningtheirbehaviour.
•TheConnersComprehensiveAssessmentScale
mayaidinitialassessmentandfollow-up
appointments.
MAP1.8.Attentiondeficithyperactivedisorder(ADHD)
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41. Psychiatry28Table1.6.Dementia
TABLE1.6.Dementia.Dementiaisasyndromeofaprogressiveglobaldeclineincognitivefunction.
TypeofdementiaCausesSignsandsymptomsInvestigationsTreatmentComplications
Alzheimer’sdiseaseExactcauseunknown.
Riskfactorsinclude:
• Down’ssyndrome
dueto↑amyloid
precursorprotein
(APP)geneload
• Familialgene
associations:
○○APP–
chromosome21
○○Presenilin-1–
chromosome14
○○Presenilin-2–
chromosome1
○○ApolipoproteinE4
(APoE4)alleles–
chromosome19
• Hypothyroidism
• Previousheadtrauma
• Familyhistoryof
Alzheimer’sdisease
• Amnesia
• Disorientation
• Changesin
personality
• Decreasingselfcare
• Apraxia
• Agnosia
• Aphasia
• Lexialanomia
• Paranoiddelusions
• Depression
• Wandering
• Aggression
• Sexualdisinhibition
Mentalstate­examination
andmini-mentalstate
examination
Addenbrooke'scognitive
examination(ACE-III)
FBC,UE,LFTs,TFTs,
CRP,ESR,glucose,
calcium,magnesium,
phosphate,VDRL,HIV
serology,vitaminB12
andfolatelevels,blood
culture,ECG,chestx-ray,
CT,MRI,SPECT
Threemainfindingson
histology:BAT
B–Betaamyloid
plaques
A–↓Acetylcholine
T–neurofibrillary
Tangles
• Memantine–
inhibitsglutamate
byblockingNMDA
receptors
• Donepezil–
acetylcholinesterase
inhibitor
• Rivastigmine–
acetylcholinesterase
inhibitor
• Amnesia
• Increasedriskof
infection
• Dysphagia
• Urinaryincontinence
• Increasedriskoffalls
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42. Psychiatry29Table1.6.Dementia
Vasculardementia• Isthesecondmost
commoncauseof
dementia
• Causedbyinfarctsof
smallandmedium
sizedvesselsinthe
brain
• Geneticassociation
withcerebral
autosomaldominant
arteriopathy
withsubcortical
infarctsand
leukoencephalopathy
(CADASIL)on
chromosome19
Followsadeteriorating
stepwiseprogression.
Therearethreetypes:
1. Vasculardementia
followingstroke
2. Multi-infarct
dementiafollowing
multiplestrokes
3. Binswanger
diseasefollowing
microvascularinfarcts
• Amnesia
• Disorientation
• Changesin
personality
• Decreasingselfcare
• Depression
• SignsofUMNlesions
(e.g.briskreflexes)
• Seizures
Mentalstate­examination
andmini-mentalstate
examination
Addenbrooke’scognitive
examination(ACE-III)
FBC,UE,LFTs,TFTs,
CRP,ESR,glucose,
calcium,magnesium,
phosphate,VDRL,HIV
serology,vitaminB12
and
folatelevels,cholesterol
levels,vasculitisscreen,
syphilisserology,ECG,
chestx-ray,CT,MRI,
SPECT
• Dietaryadvice
• Smokingcessation
• TreatDMand
hypertension
• Aspirin
Significantco-morbidity
(e.g.cardiovascular
­diseaseandrenal
disease)
Continuedoverleaf
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43. Psychiatry30Table1.6.Dementia
TABLE1.6.Dementia.Dementiaisasyndromeofaprogressiveglobaldeclineincognitivefunction(continued ).
TypeofdementiaCausesSignsandsymptomsInvestigationsTreatmentComplications
DementiawithLewy
bodies
• Associatedwith
Parkinson’sdisease
• Avoidantipsychotic
drugsinthese
patients
Isatriadof:
1. Parkinsonianism–
bradykinesia,gait
disorder
2. Hallucinations–
predominatelyvisual,
usuallyofanimals
andpeople
3. Diseaseprocess
followsafluctuating
course
Mentalstate­examination
andmini-mentalstate
examination
Addenbrooke’scognitive
examination(ACE-III)
CT,MRI,SPECT
ApoEgenotype
Lewybodies,ubiquitin
proteinsandalpha-­
synucleinfoundon
histology
• AVOID
ANTIPSYCHOTICS–
causehypersensitivity
toneuroleptics
• Levodopamay
beusedtotreat
Parkinson’ssymptoms
butthesemay
worsenpsychotic
symptoms
• Neuroleptic
hypersensitivity
• Autonomic
dysfunction
• Fluctuatingblood
pressure
• Arrhythmias
• Urinaryincontinence
• Dysphagia
• Increasedriskoffalls
Frontotemporal
­dementia(Pick’sdisease)
• Geneticassociation
withchromosome
17q21–22andtau
gene3mutations
• Amnesia
• Disorientation
• Changesin
personality
• Decreasingselfcare
• Mutism
• Echolalia
• Overeating
• Parkinsonism
• Disinhibition
Mentalstate
­examinationand
mini-mentalstate
­examination
Addenbrooke’scognitive
examination(ACE-III)
CT,MRI,SPECT
Currentlynone.Only
supportivetreatment
available.
• Increasedriskoffalls
• Increasedriskof
infection
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44. Psychiatry31Table1.6.Dementia
Histology:dependson
subtype:
1. Microvacuolartype–
microvacuolation
2. Picktype–
widespreadgliosis,
nomicrovacuolation
3. MNDtype–
histologicalchanges
likeMND
Huntington’sdementia• Causedby
Huntington’s
disease,whichisan
autosomaldominant
disorderwherethere
isadefectivegeneon
chromosome4
• Causesuncontrollable
choreiform
movementsand
dementia
Uncontrollable
­choreiformmovements
Diagnosticgenetic
testing
Nocure.Treatsymptoms:
• Chorea–anatypical
antipsychoticagent
• Obsessivecompulsive
thoughtsand
irritability–SSRIs
• Dysphagia
• Increasedriskoffalls
• Increasedriskof
infection
Continuedoverleaf
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45. Psychiatry32Table1.6.Dementia
TABLE1.6.Dementia.Dementiaisasyndromeofaprogressiveglobaldeclineincognitivefunction(continued ).
TypeofdementiaCausesSignsandsymptomsInvestigationsTreatmentComplications
Creutzfeldt–Jakob
disease(CJD)
• Causedbyprions
• Progressiveand
withoutcure
• Thereisalsovariant
CJD(vCJD),which
hasanearlieronset
ofdeath
• Rapidlyprogressive
dementia(4–5months)
• Amnesia
• Disorientation
• Changesin
personality
• Depression
• Psychosis
• Ataxia
• Seizures
EEG–triphasicspikes
seen
LP–for14-3-3protein
CT,MRI
Nocure• Increasedriskof
infection
• Coma
• Heartfailure
• Respiratoryfailure
Othercauses• HIV
• VitaminB12
deficiency
• Syphilis
• Wilson’sdisease–
autosomalrecessive
conditionwhere
copperaccumulates
withinthetissues
• Dementiapugilistica
(aka“punchdrunk”
syndrome)–seenin
boxersandpatients
whosuffermultiple
concussions
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46. TABLE2.1 UKantenatalbooking
appointments34
TABLE2.2 Thephysiologyoflabour37
TABLE2.3 Dystocia38
MAP2.1 Problemsinpregnancy39
MAP2.2 Diabetesmellitus(DM)inpregnancy40
MAP2.3 Epilepsyinpregnancy42
MAP2.4 Pre-eclampsia44
MAP2.5 Liverdiseaseuniqueto
pregnancy46
MAP2.6 TORCHESinfections50
MAP2.7 Toxoplasmosis51
MAP2.8 Rubella52
MAP2.9 Cytomegalovirus(CMV)54
MAP2.10 Herpessimplexvirus(HSV)55
MAP2.11 Humanimmunodeficiencyvirus(HIV)56
MAP2.12 Syphilis58
MAP2.13 Placentalabruption60
MAP2.14 Placentapraevia62
MAP2.15 Post-partumhaemorrhage(PPH)64
MAP2.16 Rhesusdisease66
MAP2.17 Symphysispubisdysfunction68
TABLE2.4 Breastfeeding69
ChapterTwoObstetrics
33Obstetrics
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47. 34ObstetricsTable2.1.UKantenatalbookingappointments
TABLE2.1.UKantenatalbookingappointments.Usefulwebsitethatsummarizesthecurrentprogramme:http://cpd.­
screening.nhs.uk/flashvideo/NHSPregnancyScreening.mp4.
GestationWhathappensduringtheappointment?
8–12weeksThisistheinitialbookingappointment:
• Takeageneralhistoryenquiringaboutpastmedicalmaternalhistoryandmaternallifestylefactorsincludingalcohol,smokinganddiet.
Also,askaboutfolicacidandvitaminDsupplementation.Startthesesupplementsiftheyarenotbeingtaken
• Measurebloodpressure
• Performaurinedipstickandculture(forasymptomaticbacteriuria)
• Measurepatient’sBMI
• Routinebloodtests:FBC,bloodgroup,rhesusstatus,redbloodcellalloantibodies
• Screenforinfectiousdisease:HIV,hepatitisB,rubella,syphilis
10–13+6weeks• Dateconfirmingscan
• Screensformultiplepregnancy
11–13+6weeks• Down’ssyndromescreening:thecombinedtestisofferedtowomen11–14weeksgestation.Thisconsistsofthenuchaltranslucency
scanandbloodtests(serumbetahumanchorionicgonadotropinandserumpregnancy-associatedplasmaproteinA)
16weeks• Routinebloodtest:FBC–giveironsupplementationifanaemic
• Measurebloodpressure
• Performaurinedipstickandculture
18–20+6weeks• Fetalanomalyscan
25weeksOnlyforprimiparousmothers:
• Measuresymphysis–fundalheight(SFH)
• Measurebloodpressure
• Performaurinedipstickandculture
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48. 35ObstetricsTable2.1.UKantenatalbookingappointments
28weeks• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
• Routinebloodtest:FBC–giveironsupplementationifanaemic.Checkforatypicalredbloodcellalloantibodies
• Giveanti-Dprophylaxistorhesus-negativemothers
31weeksOnlyforprimiparousmothers:
• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
34weeks• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
• Giveanti-Dprophylaxistorhesus-negativemothers
• Counselmotheraboutbirthingplanandspecificwishesorconcerns
36weeks• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
• Externalcephalicversionforbreechpresentations
• Counselmotheraboutbreastfeedingandpost-nataldepression/babyblues
38weeks• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
Continuedoverleaf
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49. 36ObstetricsTable2.1.UKantenatalbookingappointments
TABLE2.1.UKantenatalbookingappointments.Usefulwebsitethatsummarizesthecurrentprogramme:http://cpd.­
screening.nhs.uk/flashvideo/NHSPregnancyScreening.mp4(continued ).
GestationWhathappensduringtheappointment?
40weeks• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
• Counselmotheraboutinductionoflabour
41weeks• MeasureSFH
• Measurebloodpressure
• Performaurinedipstickandculture
• Counselmotheraboutinductionoflabour
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50. 37ObstetricsTable2.2.Thephysiologyoflabour
TABLE2.2.Thephysiologyoflabour.Therearethreestagesoflabourandthesuccessofeachstagedependsonmaternal,
fetalandmechanicalfactors.
StageoflabourSubcategoriesApproximatedurationSpecificinvestigations
1. Onsetofcontractionsuntil
fulldilatationofthecervix
1. Latentstage–untilthecervix
reaches 4cm
2. Activestage–from4–10cm
VariableMeasurefetalheartrateusingCTG
Measurematernalheartrate,blood
­pressureand­temperature
2. Fromfulldilatationofthe
cervixuntilthedeliveryof
thefetus
Maybesplitintoapassiveandanactive
stage.
Thefetusmechanicallyfollowsapathway
tobeexpelledfromtheuterus.
Thispathwayisasfollows:
1. Theheadbecomesengaged
2. Thefetusdescendsto‘stationzero’(the
leveloftheischialspines)
3. Headflexion
4. Headrotatesinternally
5. Headextends
6. Headrotatesexternally
7. Shouldersandbodyaresubsequently
delivered
2–3hoursMeasurefetalheartrateusingCTG
Measurematernalheartrate,blood
­pressureandtemperature
3. Fromdeliveryofthefetus
untildeliveryoftheplacenta
Noteumbilicalcordlengthening30minutesMeasurefetalresponseusingthe
APGARscore
Checkmaternalvitalsigns
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51. 38ObstetricsTable2.3.Dystocia
TABLE2.3.Dystocia.Inlayman’stermsthismeansdifficultchildbirth.Therearemanyreasonswhychildbirthmaybe
­difficult andthesemaybeclassifiedintomaternalcauses,fetalcausesandmechanicalcauses.Someexamplesare
­presentedbelow.
MaternalfactorsFetalfactorsMechanicalfactors
Ineffectiveuterinecontraction:thisoftenoccurs
innulliparouswomenwhohavehadaprolonged
labour
Maternalillness(e.g.diabetesmellitus,
­pre-eclampsia,eclampsia)
Problematicplacentalimplantation
(e.g.placentapraevia)
Fetalmalpresentation
Macrosomia:associatedwithmaternaldiabetes
Cephalopelvicdisproportion:therearefourbroad
anatomicaltypesoffemalepelvis:
• Gynecoid
• Android
• Anthropoid
• Platypelloid
Shoulderdystocia:thishasavarietyof
­associationssuchasdiabetesmellitus,macrosomia,
smallmaternalsizeandapastobstetrichistoryof
shoulderdystocia.Tomanagethisproblemseveral
manoeuvresmaybeemployedstartingwiththe
McRobert’smanoeuvre.OthersincludetheWood’s
screwprocedureandtheZavanellimanoeuvre
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52. 39ObstetricsMap2.1.Problemsinpregnancy
Disordersrelatingtohighblood
pressure
•Pre-eclampsia(seeMap2.4,p.44)
•Eclampsia
Liverdiseaseuniquetopregnancy
•Hyperemesisgravidarum(seeMap2.5,p.46)
•Intrahepaticcholestasisofpregnancy
(seeMap2.5,p.46)
•Acutefattyliverofpregnancy(seeMap
2.5,p.46)
Infections
•TORCHES(seeMap2.6,p.50)
Endocrinedisorders
•Diabetesmellitus(seeMap2.2,p.40)
Neurologicaldisorders
•Epilepsy(seeMap2.3,p.42)
MAP2.1.Problemsinpregnancy
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53. 40ObstetricsMap2.2.Diabetesmellitus(DM)inpregnancy
Whatisdiabetesmellitusinpregnancy?
Thisismetabolicconditioninwhichthepatient
hashyperglycaemiaduetoinsulininsensitivity
ordecreasedinsulinsecretion.
Causes
Thesemaybe:
Pre-existing.Therearemany–onlyafew
commoncausesarelistedhere:
•Type1DM:thisisanautoimmunecondition,
whichresultsinthedestructionofthe
pancreaticbetacellsresultinginnoinsulin
production.Thisconditionhasajuvenile
onsetandisassociatedwithHLA-DR3and
HLA-DR4.Patientsareatriskofketoacidosis.
•Type2DM:thisoccurswhenpatients
graduallybecomeinsulinresistantorwhen
thepancreaticbetacellsfailtosecrete
enoughinsulin,orboth.Itusuallyhasalater
lifeonset;however,theincidenceisincreasing
inyoungpopulationsduetoenvironmental
factorssuchasincreasingobesityand
sedentarylifestyle.Patientsareatriskof
developingahyperosmolarstate.
•Chronicpancreatitis:thisconditiondestroys
bothalphaandbetapancreaticcellssothat
glucagonandinsulinarenolongerproduced
andsecreted.
Symptoms
•General:polyuria,polyphagia,
polydipsia,blurredvision,glycosuria,signs
ofmacrovascularandmicrovasculardisease.
•Morecommonintype1DM:acetone
breath,weightloss,Kussmaul
breathing,nauseaandvomiting.
Investigations
DiagnosticinvestigationsforDMare:
•Fastingplasmaglucose:7mmol/L
(126mg/dL).
•Randomplasmaglucose(plusDMsymptoms):
11.1mmol/L(200mg/dL).
•HbA1C:6.5%.
Othertestsinclude:
•Impairedglucosetolerancetest(forborderline
cases):
Fastingplasmaglucose:7mmol/L(126
mg/dL)andat2hoursalevelof7.8–11
mmol/L(140–200mg/dL)
Plasmaglucoseat2hours:11.1mmol/L
(200mg/dL)
•Impairedfastingglucose:
Plasmaglucose:5.6–6.9mmol/L
(110–126mg/dL).
SpecifictogestationalDM:
•Oralglucosetolerancetestat16–18weeks
andat28weeksifinitialtestisnormal.
•Gestationaldiabetesmaybediagnosedwhen
thebloodglucoselevelis9mmol/L2hours
aftera75goralglucoseload.
MAP2.2.
Diabetesmellitus
(DM)inpregnancy
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54. 41ObstetricsMap2.2.Diabetesmellitus(DM)inpregnancy
andsecreted.
Treatment(gestationalDMspecific)
Conservative:
•Ensurethatmotherisunderconsultant
ledcare.
•Ensuremotheristakingahigherdoseof
folicacid(5mg/day)duetoanincreased
riskofneuraltubedefects.
•Dietcontrol.
•Increasedexercise.
Medical:
•Metformin.
•Insulin.
Complications
General:
•Macrovascular:hypertension,increasedrisk
ofstroke,myocardialinfarction,diabeticfoot.
•Microvascular:nephropathy,neuropathy
(gloveandstockingdistribution),retinopathy.
•Psychological:depression.
Fetal:
•Neuraltubeandcardiacdefects.
•Macrosomiaandshoulderdystocia.
•Neonatalhypoglycaemia.
Maternal:
•DMlaterinlife.
•Potentiallyinstrumentaldeliveryorcaesarean
section.
Gestational(i.e.itdevelopedduring
pregnancy).Thisoftennormalizesafterthebaby
isdeliveredbutmanywomengoonto
developDMlaterinlife.Theexactcauseof
gestationaldiabetesisunknown.Itisassociated
withmanyriskfactorssuchashighmaternal
BMI,ethnicoriginwithahighprevalencein
thosewithSouthAsianancestry,aprevious
historyofgestationaldiabetesoramacrosomic
baby(weight4.5kg).
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55. 42ObstetricsMap2.3.Epilepsyinpregnancy
Investigations
Notethatepilepsywilloftenbediagnosed
beforetheladyfallspregnant.However,the
followingtestsareusedtohelpaidthe
diagnosisofepilepsyandidentifythecause.
•Bloods–FBC,UE,LFTs,CRP,ESR,glucose,
calciumlevels
•Radiology–MRI
•Other–ECG,LP,EEG
Whatisepilepsy?
Thisisaconditioninwhichthebrainisaffected
byrecurrentseizures.
Causes
Seizuresarecausedbyabnormalparoxysmal
neuronaldischargesinthebrain,whichare
usuallyaresultofsomeformoftraumaticbrain
injury.Thesedischargesdisplay
hypersynchronization.Thecausesofepilepsy
maybebroadlyclassifiedintothreetypes:
1.Idiopathic–causeforepilepsyisunknown.
2.Cryptogenic–causeforepilepsyisunknown,
buttherearesignsthatsuggestthatthe
causemaybelinkedtobraininjury(e.g.
patienthasautismorlearningdifficulties).
3.Symptomatic–causeknown.Somecausesof
symptomaticepilepsyinclude:VINDICATE:
V–Vascular:historyofstroke
I–Infection:historyofmeningitisormalaria
N–Neoplasms:braintumour
D–Drugs:alcoholandillicitdruguse
I–Iatrogenic:drugwithdrawal
C–Congenital:familyhistoryofepilepsy
A–Autoimmune:vasculitis
T–Trauma:historyofbraininjury
E–Endocrine:¯Na+
,¯Ca2+
,¯or-glucose
Signsandsymptoms
Thesedependontheregionofthebrain
affected.
•Frontallobe:JAM:
J–Jacksonianmarch.
A–pAlsy(post-ictalTodd’spalsy).
M–Motorfeatures.
•Temporallobe:ADDFAT:
A–Aurathattheepilepticattackwilloccur.
D–Déjàvu.
D–Delusionalbehaviour.
F–Fear/panic–hippocampalinvolvement.
A–Automatisms.
T–Taste/smell–uncalinvolvement.
•Parietalandoccipitallobes:
Visualandsensorydisturbances
Othersinclude:partialorgeneralized
seizureswithorwithoutconvulsions,
tonguebiting,migrainesanddepression.
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56. Complications(pregnancyspecific)
General:
•Injurieswhilehavingseizure.
•Depression.
•Anxiety.
•Braindamage.
•Suddenunexplaineddeathinepilepsy
(SUDEP).
Fetal:
•Neuraltubedefects(associatedwithsodium
valproateespecially).
•Cleftpalate(associatedwithphenytoin).
•Intrauterinegrowthrestriction.
•Developmentaldelay.
Treatment(pregnancyspecific)
Continuingantiepileptictherapyduring
pregnancyisadvisablesincetherisksofhaving
seizureswhilepregnantoutweightheharmof
therapyonthefetus.
Conservative:
•Ensurethatmotherisunderconsultant
ledcare.
•Ensuremotheristakingahigherdoseoffolic
acid(5mg/day)duetoanincreasedriskof
neuraltubedefects.
Medical:
•Neonatalcare–vitaminKinjection.
•Carbamazepineisconsideredtobetheleast
teratogenicoftheolderantiepilepticagents.
•Sodiumvalproatehasthestrongest
associationwithneuraltubedefects.
MAP2.3.Epilepsyinpregnancy
43ObstetricsMap2.3.Epilepsyinpregnancy
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57. 44ObstetricsMap2.4.Pre-eclampsia
Investigations
•MonitorfetaldistressusingCTG.
•Bloods–FBC,UE,LFTs,glucose
(particularlyscreeningforHELLP
syndrome),uricacidlevel.
•Measurebloodpressure:140/90mmHg.
•Urinalysis:proteinuria.
•Neurologyexamination:hyperreflexia,clonus.
•Fundoscopy:papilloedema.
Symptoms
•Maybeasymptomatic.
•Headache.
•Visualdisturbance.
•Abdominalpain(typicallyrightupper
quadrantorepigastricregion).
•Nauseaandvomiting.
Whatispre-eclampsia?
Thisisamultisystemicdisordercharacterizedby
fourfactors:
1.Hypertension140/90mmHg.
2.Occursafter20weeksgestation.
3.Proteinuria0.3g/24hours.
4.Normalizesafterdeliveryoffetus.
Causes
Itisaplacentaldiseasebuttheexact
pathogenesisisincompletelyunderstood.
Pre-eclampsiais,however,associatedwith
numerousriskfactorssuchas:
•Extremesinage:20or40years.
•Nulliparity.
•Multiplepregnancy.
•Newpartner.
•Pasthistoryofpre-eclampsia.
•HighmaternalBMI.
•Previoushypertension.
•Previousrenaldisease.
•PreviousDM.
•Intervalbetweenpregnancies10years.
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58. 45ObstetricsMap2.4.Pre-eclampsia
Treatment
Deliveryisthedefinitivetreatmentof
pre-eclampsiabutotheroptionsareemployed
whilethefetusdevelops.Follow
NICE/consensusguidelines.
Conservative:
•Patienteducation.
•Regularbloodpressuremonitoring.
Medical:
•Labetalolisusedfirstline.
•Otheragentsincludenifedipineand
hydralazine.
•Magnesiumsulphateisalsousedforseizure
prevention.
Complications
Fetal:
•Intrauterinegrowthrestriction.
•Prematuredelivery.
Maternal:
•Eclampsia.
•HELLPsyndrome.
•Cerebralhaemorrhage.
•Intra-abdominalhaemorrhage.
MAP2.4.Pre-eclampsia
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59. 46ObstetricsMap2.5.Liverdiseaseuniquetopregnancy
Hyperemesisgravidarum
Whatishyperemesisgravidarum?
Thisisacomplicationofpregnancy,whichbeginsduringthe
firsttrimesterandusuallyresolvesbyweek20.Atriad
characterizesthecondition:
1.Nauseaandvomiting.
2.Weightloss(5%ormoreofpre-pregnancybodyweight).
3.Dehydration.
Causes
Theexactcauseisunknown.
Symptoms
•Nauseaandvomiting.
•Weightloss(5%ormoreofpre-pregnancybodyweight).
•Dehydration–resultinginketosisandconstipation.
•Metabolicimbalance–ketosisandthyrotoxicosis.
•Hyperolfaction.
•Ptyalism.
Investigations
•MonitorfetaldistressusingCTG.
Intrahepaticcholestasisofpregnancy
Whatisintra-hepaticcholestasisofpregnancy?
Thisisareversiblehormonallyinfluencedcholestasis,which
typicallypresentsduringthesecondtrimesterandcontinues
intothethirdtrimester.
Causes
Theexactcauseisunknown.Studieshavesuggestedthatthis
conditionislinkedtoincreasedhormonelevels.Increased
riskwithmultiplepregnancies.Thisconditionoftenrecursin
subsequentpregnancies.
Symptoms
•Pruritus,typicallycommencingonthepalmsofthehands
andsolesofthefeet.Itchingthenspreadstothefaceand
trunk.Worseatnight.Norashpresent.
•Jaundice.
•Steatorrhoea.
Investigations
•MonitorfetaldistressusingCTG.
MAP2.5.Liverdiseaseuniqueto
pregnancy
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60. 47ObstetricsMap2.5.Liverdiseaseuniquetopregnancy
•Bloods–FBC,UE,BUN,TFTs(TSHlow),LFTs=AST,
ALT1,000IU/L,ALTAST,vitaminBlevels.
•Urinalysis.
•USS–monitorgestationandexcludemolarpregnancy
(seeMap3.3,p.76).
Treatment
Medical:
•IVfluidresuscitation.
•Antiemetics–pyridoxine,promethazine.
•Nutritionalsupport–thiamine.
Complications
Mother:
•Weightloss.
•Complicationsofvomiting(e.g.oesophagealrupture,
renaldamage,vasculardepletion,Wernicke’s
encephalopathy).
Fetus:
•Prematurity.
•Lowbirthweight.
•Bloods–FBC,UE,BUN,LFTs=AST,ALT1,000IU/L,
GGTnormal,bileacidlevels(high),prothrombin
(normal),bilirubin6mg/dL.
•Urinalysis.
•USS–monitorgestation.
Treatment
•Medical:ursodeoxycholicacid,antihistamines.
•Deliveryoffetus(usuallyat37weeksorwhenfetal
distressisimminent).
Complications
Mother:
•Severepruritus–interfereswithsleep.
•Derangedclotting–duetodecreasedvitaminKlevels.
Fetus:
•Fetaldistress.
•Stillbirth.
•Meconiumingestion/aspiration.
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61. 48ObstetricsMap2.5.Liverdiseaseuniquetopregnancy
Acutefattyliverofpregnancy
Whatisacutefattyliverofpregnancy?
Thisisaseriouscomplicationofpregnancythattypicallyoccursinthethirdtrimester.Itischaracterizedbymicrovesicular
steatosis(variantformofhepaticfataccumulation)intheliver.Associatedwitheclampsia.
Causes
Theexactcauseisunknown.Increasedriskinwomenwhohaveaheterozygouslong-chain3-hydroxyacylcoenzyme
Adehydrogenase(LCHAD)deficiency.Thisconditionisthoughttobeduetomitochondrialdysfunction.Dysfunctionofthe
mitochondriaresultsinthedysfunctionoffattyacidoxidationand,assuch,anaccumulationoffatwithinthehepatocytes.
Excessfatinfiltrationresultsinacutehepaticinsufficiency.
Symptoms
•Non-specific–lethargy,nauseaandvomiting.
•Hypertension.
•Abdominalpain–epigastric,RUQ.
•Symptomsassociatedwith:uppergastrointestinalhaemorrhage,acutekidneyinjury,pancreatitis,hypoglycaemia,fulminant
hepaticfailure.
•Encephalopathy–alteredmentalstatusandconfusion.
•Jaundice.
Investigations
•MonitorfetaldistressusingCTG.
MAP2.5.Liverdiseaseuniquetopregnancy(continued).
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62. 49ObstetricsMap2.5.Liverdiseaseuniquetopregnancy
•Bloods–FBC,platelets100,000mm3
,fibrinogenlevel(low),antithrombinIII,UE,BUN,LFTs=AST,
ALT300IU/L,prothrombin(increased),bilirubin(increased),DIC,glucoselevels(decreased).
•Urinalysis.
•MaternalUSS–liver(increasedechogenicity).
•FetalUSS–monitorgestation.
Treatment
Medical:
•Resuscitation–IVfluids,IVglucose,freshfrozenplasma,cryoprecipitate.
•Deliveryoffetus.
Surgical:
•Livertransplantmayberequiredformotherswithsevereliverfailure,encephalopathyorsevereDIC.
Complications
Mother:
•Fulminanthepaticfailure.
•DIC.
•Encephalopathy.
•Death20%.
Fetus:
•Fetalmortality~45%.
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63. 50ObstetricsMap2.6.TORCHESinfections
Syphilis
(SeeMap2.8,p.52)
TO–TOxoplasmosis
R–Rubella
C–CMV
HE–HErpesandHIV
S–Syphilis
Herpessimplexvirus(HSV)
(SeeMap2.11,p.56)
Humanimmunodeficiencyvirus(HIV)
(SeeMap2.10,p.55)
Toxoplasmosis
(SeeMap2.7,p.51)
Cytomegalovirus(CMV)
(SeeMap2.9,p.54)
Rubella
(SeeMap2.12,p.58)
MAP2.6.TORCHESinfections
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64. 51Obstetrics
Treatment
Conservative:
•Patienteducation.
•Advisepregnantwomentoavoidcats/clearinglittertrays.
•Donotallowpetcattosleepinsamebed.
•Highlighthandhygiene,especiallyifhandlingrawmeat.
Medical:
•Fetal:
Pyrimethamine.
Sulphonamide.
•Maternal:
Spiramycin.
Whatistoxoplasmosis?
Thisisaninfectioncausedby
Toxoplasmagondii,aprotozoan.Infectionismore
commoninimmunosuppressedindividuals
(e.g.HIV,cancersufferers).
Transmission:
•Infectedmeat.
•Catfaeces.
Symptoms
•Oftenasymptomatic.
•Flu-likesymptoms–fatigue,sore
throat,headache,fever,
lymphadenopathy.
Investigations
•Bloodtest:maternal
immunoglobulinM.
•Radiology:ultrasound
scanforfetalhydrocephalus.
•Amniocentesis.
•Performadditionaltests
(e.g.forHIVco-infection
ifclinicallyrelevant).
Complications
Fetal:Rememberasthe3Cs:
C–Cerebralmanifestations
(e.g.hydrocephalus,microcephaly).
C–Convulsions.
C–Chorioretinitis.
Maternal:RememberasABCDE:
A–Abscessformation(cerebral)
B–Blurredvision
C–Confusion
D–Difficultybreathing(pneumonitis)
E–Encephalomyelitis
MAP2.7.Toxoplasmosis
Map2.7.Toxoplasmosis
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65. 52ObstetricsMap2.8.Rubella
Symptoms
•Arthralgia.
•Sorethroat.
•Fever.
•Macularrash–initiallyonfacebutspreadsto
torsoandthenlegs.Durationabout3days.
•Occipitallymphadenopathy;thismaybe
painfulandcausediscomfort.
Whatisrubella?
ThisisasinglestrandedRNAvirus.Itisalso
knownasGermanmeasles.Greatestriskof
infectionandcomplicationsisduringthefirst
fewweeksofpregnancy.
Transmission:
•Airborneinfectionpassedthrough
respiratorydroplets.
Investigations
•Bloodtest:maternalantibodies.
•Urinalysis:forvirusinneonate.
MAP2.8.Rubella
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66. 53ObstetricsMap2.8.Rubella
Complications
Fetal:
•Congenitalrubellasyndrome-rememberas
ABCDE:
A–Asmallhead(microcephaly)andlowbirth
weight
B–Blueberrymuffinrash(extramedullary
haematopoiesis)
C–Congenitalheartmalformations(PDA,PAS)
D–Deafness(sensorineural)
E–Eyeabnormalities(cataracts)
Maternal:asinSymptomsbox.
Treatment
Thereisnospecifictreatmentforrubella.
Conservative:
•Patienteducation.
•Advisepregnantwomentoavoidknown
contactswithrubella(e.g.knowncasesat
work).
Medical:
•Maternal:
MMRvaccine.
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67. 54ObstetricsMap2.9.Cytomegalovirus(CMV)
WhatisCMV?
Thisisanenvelopedvirusbelongingtothe
Herpesviridaefamily.
Transmission:
•Airborneinfectionpassedthroughrespiratory
droplets.
•Viamaternalgenitourinarytract.
Investigations
•Bloodtest:maternalantibodies.
•Radiology:USSmayshowhyperechogenicbowel.
•Hyperechogenicbowelisalsofoundincysticfibrosis
andDown’ssyndrome.
Symptoms
•Generallyasymptomatic.
MAP2.9.Cytomegalovirus(CMV)
Complications
Fetal:rememberasABCDE:
A–Asmallheadmicrocephaly)andlowbirthweight
B–Blindness(occasionally)
C–Causesneonataljaundice
D–Deafness(highrisk)
E–Enlargedliverandspleen
Maternal:asinSymptomsbox.
Treatment
ThereisnospecifictreatmentforCMV.
ThemedicationsusedtotreatCMVordinarilyare
teratogenic.
Conservative:
•Patienteducation.
Medical:
•Maternal:
Considerterminationofpregnancy.
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68. 55ObstetricsMap2.10.Herpessimplexvirus(HSV)
WhatisHSV?
ThisisavirusbelongingtotheHerpesviridae
family.Therearemanydifferenttypesofherpes
virus,butthismindmapfocusesonHSV-1and
HSV-2.
Transmission:
•Sexualcontact.
•Mucousmembranecontact(e.g.saliva).
Investigations
•Viralswab.
•ViralPCR.
Symptoms
•Tenderblister(s)thatoccureitheron
theliporinthegenitalregion.These
mayweep.
•Lymphadenopathy.
Treatment
Conservative:
•Patienteducation.
•Adviseondeliveryroute(i.e.caesarean
sectionispreferable).
Medical:
•Maternal:aciclovir.
•Fetal:aciclovir.
Complications
Fetal:rememberasABCDE:
A–Asmallhead(microcephaly)
B–Brainpathology(meningitis)
C–Chorioretinitis
D–Death
E–Encephalitis
Maternal:asinSymptomsbox.
MAP2.10.Herpessimplexvirus(HSV)
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69. 56ObstetricsMap2.11.Humanimmunodeficiencyvirus(HIV)
WhatisHIV?
ThisisanRNAretrovirusoftheLentivirusgenus.
Thisviruscausesacquiredimmunodeficiency
syndrome(AIDS).
Cause
TherearetwotypesofHIV:
•HIV-1:
○GroupM,subtypesAtoJ:prevalentin
Europe,NorthAmerica,Australiaand
sub-SaharanAfrica.
○GroupO:mainlyinCameroon.
•HIV-2:
○PredominantlyconfinedtoWestAfrica.
Transmission
•Unprotectedsexualintercourse.
•Sharedneedles(e.g.drugusers).
•Contaminatedbloodtranfusions.
•Verticaltransmission–mothertochild.The
viruscrossestheplacentaandistransmitted
throughbreastmilk.
MAP2.11.Humanimmunodeficiencyvirus(HIV)
Investigations
•Enzyme-linkedimmunosorbentassay(ELISA).
•Westernblottest.
•Immunofluorescenceassay(IFA).
•Nucleicacidtesting.
Genesrequiredforviralreplication
PEG:
P–pol:encodesreversetranscriptaseand
integrase
E–env:encodesenvelopeproteins(e.g.gp120)
G–gag:encodesviralstructuralproteins.
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70. 57ObstetricsMap2.11.Humanimmunodeficiencyvirus(HIV)
Treatment
Conservative:
•Patientadvice,plannedcaesareandelivery,infantbottlefeeding.
Medical:
•Highlyactiveantiretroviraltherapy(HAART):
○Nucleosidereversetranscriptaseinhibitors(NRTIs)(e.g.zidovudine[particularlytoreduce
verticaltransmission]).Note:Zidovudineistheonlyagentshowntodecreaseperinatal
transmission.
○Non-nucleosidereversetranscriptaseinhibitors(NNRTIs)(e.g.nevirapine).
○Proteaseinhibitors(PIs)(e.g.atazanavir).
•Giveeither:
○TwoNRTIscombinedwithoneNNRTI;or
○TwoNRTIscombinedwithonePI;or
○TwoNRTIscombinedwithoneintegraseinhibitor(II;e.g.raltegavir).
Specialnotes:
•NRTIscrosstheplacenta,theNNRTIsnevirapineandefavirenzcrosstheplacenta,butPIsdonot
crosstheplacentaeasily.
•Zidovudineisgivenintravenouslyduringlabour.
•Neonatalcare:infantzidovudine,initiatedassoonaspossibleafterdeliveryandcontinueduntil
6weeks.
•HepatitisBco-infections:tenofovirandlamivudineoremtricitabine.
Complications
Fetal:
•IUGR.
•Stillbirth.
Maternal:
•Pre-eclampsia.
•Increasedriskofinfection:
○Toxoplasmosis.
○CMVretinitis.
○Pneumocysticjiroveciipneumonia.
○Kaposi’ssarcoma.
○Cryptococcalmeningitis.
○Mycobacteriumaviumcomplex.
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71. 58ObstetricsMap2.12.Syphilis
Whatissyphilis?
Thisisasexuallytransmitteddiseasecausedby
thespirochaeteTreponemapallidum.
Transmission:
•Sexualcontact.
Symptoms
Infectionsoccursinthreestages:
1.Chancre–painless.
2.Disseminateddisease–rashonpalms
andsoles.
3.Cardiacandneurologicalinvolvement.
Investigations
•VenerealDiseaseResearchLaboratory
(VDRL)test.
•Rapidplasmareagintest.
•Fluorescenttreponemalantibodyabsorption
test(FTA-ABS).
•Treponemapallidumhaemagglutinationtest
(TPHA).
•Treponemapallidumparticleagglutination
test(TPPA).
•Treponemalenzymeimmunoassay(EIA).
MAP2.12.Syphilis
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72. 59ObstetricsMap2.12.Syphilis
Treatment
Conservative:
•Patienteducation.
•Adviseondeliveryroute(i.e.caesareansectionispreferable)
Medical:(manyantibioticslistedbelowarecontraindicatedduring
pregnancy.ConsultlocalguidelinesandtheBNF).Mothermayneedto
considerterminationofpregnancy.
•Maternal:
ProcainepenicillinG.
Doxycycline.
Erythromycin.
Azithromycin.
Note:Ifpatienthasneurosyphilis,giveprophylacticprednisoloneto
avoidtheJarisch–Herxheimerreaction.Thisreactionmayoccurafter
antibacterialtreatment,whichcausesthedeathofthespirochaeteand
subsequentendotoxinrelease.EndotoxinscausetheJarisch–Herxheimer
reaction.
•Fetal:
Penicillin.
Complications
Fetal:ABCDES:
A–Asmallhead(microcephaly)
B–Brainpathology(meningitis),Bloodstainednasaldischarge
C–Choroiditis
D–Dentalmalformations,Deafness(sensorineural)
E–Enlargedliverandspleen
S–Skinlesions,Seizures
Maternal:
•Miscarriage.
•Gummaformation.
•Meningitis.
•Stroke.
•Heartvalvedamage.
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73. 60ObstetricsMap2.13.Placentalabruption
Whatisplacentalabruption?
Thisisacauseofantepartumhaemorrhage,which
maybedefinedasvaginalbleedingthatoccursat24
weeksgestation.Thecausesofantepartum
haemorrhagemayberememberedasPVC2
:
P–Placentalabruption
P–Placentapraevia
V–Vasapraevia
V–Vaginalinfection
C–Cancerofthecervix
C–Cervicitis
Causes
Placentalabruptionoccurswhentheplacenta
separatesfromthewalloftheuterus.Itis
subclassifiedaseitheraconcealedorrevealed(more
common)abruption.
Riskfactors
RememberasOHPIPS:
O–Overdistendeduterus
H–Hypertension
P–Pre-eclampsia
I–Intra-uterinegrowthrestriction
P–Pasthistoryofplacentalabruption
S–Smokinghistory
Symptoms
•Vaginalbleeding.
•Severeabdominalpainoutofkeeping
withbloodloss,coupledwithsignsof
systemicshockmayindicateconcealed
abruption.
•Woodenuterusonpalpation.
Investigations
•MonitorfetaldistresswithCTG.
•Bloodtests:FBC,UE,groupandsave.
•Radiology:USSforplacentapraevia.
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74. 61ObstetricsMap2.13.Placentalabruption
Treatment
Medical:
•Emergencytreatment:admission,cross-match
andbloodtransfusion.
•Considerdeliverydependingongestation.If
thefetusis34weeks,givingsteroidstothe
motherwillhelpinducefetallung
development.
Complications
Fetal:
•Death
•Intra-uterinegrowthrestriction
Maternal:DADS:
D–Death
A–Acutekidneyinjury
D–Disseminatedintravascular
coagulationandmulti-organfailure
S–Shock
MAP2.13.Placental
abruption
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75. 62ObstetricsMap2.14.Placentapraevia
Whatisplacentapraevia?
Thisisa‘lowlyingplacenta’andacauseof
antepartumhaemorrhage,whichmaybedefinedas
vaginalbleedingthatoccursat24weeksgestation.
Othercausesofantepartumhaemorrhagearelisted
inMap2.13,p.60.
Placentapraeviamaybeclassifiedaseither
minorormajor.Themajorformcompletelycovers
theinternalos,whereasintheminorformthe
internalosisonlypartiallycovered.
Causes
Placentapraeviaiscausedbylowimplantationof
theembryo.
Riskfactors
RememberasMUMS:
M–Maternalage
U–Uterineabnormality
M–Multiparity
S–Section(caesarean)
Symptoms
•Painlessvaginalbleeding.
•Abnormalfetallie/failureofengagement.
Investigations
•MonitorfetaldistresswithCTG.
•Bloodtests:FBC,UE,groupandsave.
•Radiology:abdominalandtransvaginalUSS.
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76. 63ObstetricsMap2.14.Placentapraevia
Treatment
Medical:
•Emergencytreatment:admission,cross-match
andbloodtransfusion.
•Considerelectivecaesareansectiondepending
ongestation.Ifthefetusis34weeks,giving
steroidstothemotherwillhelpinducefetallung
development.
Complications
Fetal:
•Death
•Prematuredelivery.
Maternal:
•Massivehaemorrhageanddeath.
•Hysterectomy.
•Highriskofpost-partumhaemorrhage.
MAP2.14.Placenta
praevia
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77. 64ObstetricsMap2.15.Post-partumhaemorrhage(PPH)
WhatisPPH?
Thisisbleedingthatoccursafterdeliveryofthefetus.Itmaybedefinedasprimary,secondaryor
massivedependingontheamountofbloodlostandthetimethathaselapsedpostdelivery.
Causes
Primary:rememberasthe5Ts:
T–Toneofuteruslost(mostcommoncause)
T–Trauma(e.g.toperineumoruterinerupture)
T–Torncervixorvagina
T–Thrombin(i.e.bleedingdisorders)
T–Tissue(i.e.retainedproductsofconception)
Secondary:
•Infection–endometritis.
•Retainedproductsofconception.
Riskfactors:rememberasABCD:
A–Antepartumhaemorrhage
B–Birthingproblems(i.e.instrumentaldelivery,inducedlabour)
C–Coagulationdisorders(e.g.vonWillebranddisease)
D–Durationoflabour12hours
TypeofPPHBloodlostTimeelapsedafterbirth
Primary500mL24hours
Secondary500mL24hoursto12weeks
Massive1,500mLN/A
Symptoms
DependsonthecauseofPPH.Allmay
presentwithshock:
•Atonicuterus:uterusisenlarged.
•Uterinerupture:abdominalpain,vaginal
bloodloss.
•Infection:tachycardia,fever,abdominal
pain,vaginalbloodloss.
•Retainedconceptionproducts:signsof
infection(seeabove).
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78. 65ObstetricsMap2.15.Post-partumhaemorrhage(PPH)
Treatment
Emergencytreatment:
•Generallyresuscitationmanagement
includinganABCDEapproachwith
insertionoftwowideborecannulas.
•Bloods:cross-matchandbloodtransfusion.
•Specificmanagementdependingoncause:
Atonicuterus:uterinemassage.
Uterinerupture:laparotomy.
Endometritis:antibiotics(checklocal
guidelines).
Retainedproductsofconception:
evacuationwithsuctioncurette.
Investigations
•TraumaABCDEwithurineoutput
measurement.
•Identifycause(e.g.vaginalexamination).
•MonitorfetaldistresswithCTG.
•Bloodtests:FBC,UE,groupandsave.
•Radiology:abdominalandtransvaginal
USS.
Complications
•Massivehaemorrhage.
•Hysterectomy.
•Death.
MAP2.15.Post-partumhaemorrhage(PPH)
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79. 66ObstetricsMap2.16.Rhesusdisease
Whatisrhesusdisease?
Thisdiseaseisonecauseofhaemolyticdisease
ofthenewborn.Antibodiesfroma
rhesus-negativemotherdestroyfetalblood
cells,resultinginhaemolyticdisease.
Causes
Rhesusdiseaseoccursasadirectresultof
maternalantibodiesattackingfetalbloodcells.
Thishappenswhenthemotherisrhesus
negativebutthefetusisrhesuspositive.
Themothermusthavebeenpreviously
sensitized(byexposuretorhesus-positiveblood
[e.g.duringapreviouspregnancy]).
Investigations
•Rhesusstatusisdiagnosedduringtheroutine
UKscreeningprogramme(seeTable2.1,p.34).
•Coombstest–bloodsamplingfromthe
umbilicalcordassessesbaby’sbloodtypeas
wellaswhetheranti-Dantibodieshave
passedintothebaby’sblood.
Symptoms
Symptomsdependontheseverityofrhesus
disease.
Generalsymptoms:
•Hypotonia.
•Offfeeds.
•Haemolyticanaemia(ofvaryingseverity).
•Jaundice(ofvaryingseverity).
Mildanaemia
Moderatejaundice
Moderate
Severeanaemia
Hydropsfoetalis
Hypoglycaemia
Moderateanaemia
Moderate–severejaundice
Mild
Severe
BloodlostTimeelapsedafterbirth
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80. 67ObstetricsMap2.16.Rhesusdisease
Treatment
Medical:
•Preventingrhesusdisease:
Routineantenatalanti-Dprophylaxis:
1.Singledosetreatment–at28–30
weeks.
2.Doubledosetreatment–at28
weeksand34weeks.
Anti-Dimmunoglobulingivenatany
sensitizingevent(e.g.anybleeding).
Anti-Dimmunoglobulingivenwithin
72hoursafterbirthifmotherhas
notbeensensitized.
•Treatingrhesusdisease:
Phototherapy.
Intravenousimmunoglobulin.
Bloodtransfusions.
Complications
•Haemolyticdiseaseofthenewborn.
•Stillbirth.
•Learningdifficulties.
•Deafness.
•Blindness.
MAP2.16.Rhesusdisease
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81. 68ObstetricsMap2.17.Symphysispubisdysfunction
Whatissymphysispubisdysfunction?
Thisisaconditionofpainanddiscomfortthat
occursinsomepregnantwomendueto
increasedmovementandmisalignmentofthe
pelvicbonesatthepubissymphysis.Symptoms
tendtoworsenasthepregnancyprogressesand
thereisanincreasedriskwithmultiparity.
Causes
Duetoincreasedlaxityofthepelvicligaments.
Thisoccursduetoincreasedrelaxinhormone
levels.
Investigations
•Usuallyaclinicaldiagnosis.
•Radiology–USSmaybeusedtoassessthe
degreeofseparationatthepubicsymphysis.
9mmisconsideredphysiologicalin
pregnancy;10mminpregnancyis
consideredpathological.
Symptoms
•Painandpelvicdiscomfort(typicallyatthe
pubicsymphysisbutmayalsooccuratthe
sacroiliacjoints).
•Painworsenswithmovementandcertain
activitiessuchasclimbingstairs.
•Waddlinggait.
•Palpation–tendernessoverthepubic
symphysis;agapmaybefelt.
Treatment
Conservative:
•Physiotherapy.
•Placeapillowbetweenthelegswhileinbed
resting.
•Avoidactivitiesthatworsenthepain.
Medical:
•Analgesia:paracetamol.
Complications
•Diastasisofthesymphysispubis.
MAP2.17.Symphysis
pubisdysfunction
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82. 69ObstetricsTable2.4.Breastfeeding
TABLE2.4.Breastfeeding.
AdvantagesDisadvantagesAbsolutecontraindications
Benefitsforbaby:
• Decreasedriskofinfection(e.g.chestinfection,
earinfection,urinarytractinfection)
• Decreasedriskofasthma
• Decreasedriskofeczema
• Decreasedriskofdiabetesmellitus
• Decreasedriskofdiarrhoeaandvomiting
Benefitsformother:
• Decreasedriskofcancer:breastandovarian
• Decreasedriskofosteoporosis
• Increasedbondingwithchild
• Verticaltransmission
• Riskofmastitis
• Motherrequiresadditionalcalories
• Verticalinfections(e.g.HIV)
• Galactosaemia
• Drugs:rememberABCS:
A–Antibiotics(e.g.tetracyclines)
A–Aspirin
A–Amiodarone
B–Benzodiazepine
C–Cytotoxicdrugs
C–Carbimazole
S–Sulphonylureas
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83. K30033_C002.indd 70 28/02/17 11:16 am

84. ChapterThreeGynaecology
MAP3.1 Ectopicpregnancy72
MAP3.2 Miscarriage74
MAP3.3 Molarpregnancies76
TABLE3.1 Sexuallytransmittedinfections78
TABLE3.2 Non-sexuallytransmitted­infections80
TABLE3.3 Menorrhagia81
MAP3.4 Amenorrhoea82
MAP3.5 Polycysticovary
syndrome(PCOS)84
TABLE3.4 Terminationofpregnancy(TOP)86
MAP3.6 Infertility88
MAP3.7 Cervicalcancer90
MAP3.8 Vaginalcancer92
MAP3.9 Endometrialcancer94
MAP3.10 Ovariancancer96
TABLE3.5 Ovariancysts98
TABLE3.6 Incontinence99
TABLE3.7 Contraception100
Gynaecology71
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85. Gynaecology72Map3.1.Ectopicpregnancy
Whatisanectopicpregnancy?
Thisiswhentheembryoimplantsoutsidethe
uterus.Theembryomayimplantinthe
abdomenbutmoreoftenitisatubalpregnancy
mostcommonlylocatedintheampullaregion
ofthefallopiantube(80%).
Causes
Anythingthatnarrowsordamagesthe
fallopiantubemayresultinanectopic
pregnancy.
RememberasTIPS:
T–Theprogesteroneonlypill–resultsin
thickenedsecretions.
I–InfectionandIVFtreatment.
P–Pelvicinflammatorydisease.
S–Surgicalprocedures–resultinadhesions.
Investigations
•Pregnancytestandb-hCGlevels.
•Bloodtests:FBC,UE,groupandsave.
•Radiology:transvaginalUSS.
Symptoms
Considerinanysexuallyactivefemalewhohas
abdominalpainandwhohasmissedaperiod:
•Abdominalpain–usuallyinthelowerright
orlowerleftquadrantsandcolickyinnature.
•Vaginalbleeding–darkcolouredand
likenedto‘prunejuice’.
•Nauseaandvomiting.
•Signsofshock:clammyappearance,pale,
tachycardic,hypotensive.
•Vaginalexamination:cervicalexcitation.
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86. Complications
RememberasTUBE:
T–Tubalrupture.
U–sUbfertility.
B–Blues(i.e.psychologicalimplicationsrelated
tochildlossandpossiblesubfertility).
E–Ectopicpregnancyriskincreasesfor
subsequentpregnancies.
Treatment
Emergencytreatment
Dependsoninitialpresentation:
•Generalresuscitationmanagement
includinganABCDEapproachwithinsertion
oftwowideborecannulas.
•Bloods:cross-matchandbloodtransfusion.
•Consideranti-Dprophylaxis.
Medical:
•Methotrexate.
Surgical:
•Laparoscopicsalpingotomy/salpingectomy.
•Ifthisfails,thenconsiderlaparotomy.
MAP3.1.Ectopicpregnancy
73Map3.1.EctopicpregnancyGynaecology
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87. Gynaecology74Map3.2.Miscarriage
Investigations
•b-hCGlevels.
•Bloodtests:FBC,UE,groupandsave,
rhesusstatus.
•Radiology:transvaginalUSS.
Whatisamiscarriage?
Thisiswhenthefetusis
spontaneouslyaborted24weeks
gestation,withthemajoritybeing
12weeksgestation.Thereare
manydifferenttypesof
miscarriage.Thesemaybedefined
aseithercompleteorincomplete,
orclassifiedaccordingtotheir
presentation,suchasinevitable,
threatened,missedandrecurrent.
Causes
Mostlythecauseisunknownbut
broadcauses,particularlyofrecurrent
miscarriage,mayberemembered
asABC:
A–Antiphospholipidsyndrome,
increasingAge
B–Bleedingdisorders(e.g.von
Willebranddisease)
C–Chromosomalabnormality,
Cervicalincompetence
Typeof
miscarriage
Symptoms
Cervicalos
openorclosed
Inevitable
Threatened
Missed
Heavyvaginalbleeding
Abdominalpain
Lightvaginalbleeding
Fetusmaysurvive
Novaginalbleeding
Fetusisnolongerviable
Open
Closed
Closed
Symptoms
Symptomsdependonthetypeofmiscarriage.
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88. Gynaecology75Map3.2.Miscarriage
Treatment
•Dependsonclinicalpresentationandthe
typeofmiscarriage.
Emergencytreatment:
•Mayberequiredifmotherishaemorrhaging.
Medical:
•Prostaglandins+/–mifepristone
(anti-progesterone).
Surgical:
•Suctioncurettage.
Complications
•Infectionandpyrexia.
•Psychologicalimplicationsincluding
depression.
•Complicationofsurgicalcurettage(e.g.the
riskassociatedwithgeneralanaesthetic,
uterineperforation,Asherman’ssyndrome
[intrauterineadhesions]).
MAP3.2.Miscarriage
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89. Gynaecology76Map3.3.Molarpregnancies
Whatisamolarpregnancy?
Molarpregnancies,alsoknownasgestationaltrophoblastic
disease,areduetoexcessiveuncontrolledproliferationof
trophoblastictissue.Theymaybecharacterizedaseither
partialorcompletemolarpregnanciesandfurther
characterizedasbenignormalignant.
Typeofmolarpregnancy
Hydatidiformmole
Invasivemole
Benignormalignant?
Choriocarcinoma
Benign
Malignant
Malignant
Causes
•Partialmolesaremadefrombothmaternalandpaternal
geneticmaterial.
•Completemolesaremadefromonlypaternalgenetic
material.
Riskfactors
•Extremesofmaternalage.
•MorecommoninwomenofAsianancestry.
Investigations
•b-hCGlevels:excessivelyhigh.
•Bloodpressure.
•Bloodtests:FBC,UE,TFTs(groupand
save,rhesusstatusifexcessive
bleeding).
•Radiology:transvaginalUSS–a‘snow
storm’appearanceispathognomonic.
Symptoms
•Uteruslargefordates.
•Vaginalbleeding.
•Hyperemesis.
•Raresymptoms:pre-eclampsia,
hyperthyroidism.
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90. Gynaecology77Map3.3.Molarpregnancies
Treatment
Conservative:
•Patienteducation.
•Contactspecialistcentresfortrophoblasticdisease.
Medical:
•Prostaglandins+/–mifepristone(anti-progesterone)
sometimesusedtoaidremovaloftrophoblastictissue.
•Chemotherapymayberequired.
Surgical:
•Suctioncurettage.
Complications
•Increasedriskoftrophoblasticdiseaseinsubsequent
pregnancies.
•Trophoblasticdiseasemaybecomepersistentandrequire
chemotherapy.
•Choriocarcinomamaymetastasize.
MAP3.3.Molarpregnancies
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91. Gynaecology78Table3.1.Sexuallytransmittedinfections
TABLE3.1.Sexuallytransmittedinfections.
DiseaseCausative
organism
SymptomsInvestigationsTreatment
ChlamydiaChlamydia
­trachomatis
• Asymptomatic(thereiscurrentlyan
opportunisticscreeningprogrammeinthe
UKforunder25’s)
• Females:vaginaldischarge,inter-menstrual
orpost-coitalbleeding,cervicitis
• Males:urethritis,dysuria
• Itisthemostcommoncauseofpelvic
inflammatorydisease
Nucleicacidamplification
test(NAAT)fromeither
endocervicalswabs/urine
sampleforwomenanda
urinesampleformen
• Doxycycline(7days)
• Azithromycin(singledose)
TrichomoniasisTrichomonas
vaginalis
• Asymptomatic
• Females:vaginaldischarge(greenand
offensive),vulvovaginitis,‘strawberry
cervix’,superficialdyspareunia,pH4.5
• Males:urethritis
Wetmountmicroscopyto
visualizemotiletrophozoites
• Metronidazole
GonorrhoeaNeisseria
­gonorrhoeae
• Females:generallyasymptomatic,vaginal
discharge,cervicitis
• Males:urethritis
Endocervicalswabs• azithromycinandIM
ceftriaxone
Genitalwarts
(condylomata
­accuminata)
Human
­papillomavirus
(HPV)
• Papilliformorflatwarts
• Maybepigmented
• Maybleed
• Mayitch
Clinicalpresentation• Firstline–topical
podophyllumorcryotherapy
• Secondline–imiquimod
cream
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92. Gynaecology79Table3.1.Sexuallytransmittedinfections
GenitalherpesHerpessimplex
virus(HSV)1and2
• Painful,ulceratedlesions
• Dysuria
• Lymphadenopathy
Viralswab• Aciclovir
SyphilisTreponema
­pallidum
SeeMap2.12(p.58)
Splitinto:
• Primarysyphilis–chancre
• Secondarysyphilis–rash
• Tertiarysyphilis–cardiacandneurological
involvement.Gummataformation
SeeMap2.12(p.58)
VDRLtesting
• Penicillin
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93. Gynaecology80Table3.2.Non-sexuallytransmittedinfections
TABLE3.2.Non-sexuallytransmittedinfections.
DiseaseCausative
­organism
SymptomsInvestigationsTreatment
CandidiasisCandida­albicans• Typicaldischarge(‘cottage
cheese’)
• Itching
• Vulvitis
• Microscopyandculture• Topicalpreparations
(e.g.imidazoles)
• Oralpreparations
(e.g.fluconazole)
BacterialvaginosisGardnerella
vaginalis
• Maybeasymptomatic
• Amsel’scriteria–threeofthe
fourcriterialistedbelowmust
bemet:
1. Whitehomogeneousdischarge
2. Cluecellsvisibleonmicroscopy
3. VaginalpH4.5
4. Positivewhifftest–afishy
odouriscreatedonadditionof
potassiumhydroxide
• RefertoAmsel’scriteria:
microscopy,increased
vaginal pH,additionof
potassiumhydroxide
• Oralmetronidazole
(5–7days)
• Secondline–topicalmetronidazoleor
clindamycin
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94. Gynaecology81
TABLE3.3.Menorrhagia.Inlayman’sterms,menorrhagiaisheavymenstrualbleeding.Previouslyitwasdefined
­objectively as80mLbloodloss;however,therehasbeenashifttothesubjectivewhereheavymenstrual
bleedingisdefinedbywhatthewomanfeelsisexcessive.
CausesInvestigationsTreatment
RememberasUBLEED:
U–Uterinepolyps/Uterinefibroids
B – Bleedingdisorders(e.g.vonWillebrand
disease)
L – Likelynounderlyingpathology(50%)
E – Endometriosis
E – Endometrialcarcinoma/hyperplasia
D– pelvicinflammatoryDisease/
intrauterineDevices
Dependsonthecauseofmenorrhagia.Itisessential
toperformanFBCineachcasetoexcludeanaemia.
Someinvestigationsarelistedbelow:
• Generalbloodtests:FBC,UE,TFTs
• Radiology:USS,hysteroscopy,endometrialbiopsy
ifindicated
Refertoappropriatelocalalgorithms.
Treatmentisastepwiseapproach.
Medical:
• First-line:Mirenaintrauterinesystem
• Second-line:mefenamicacid(particularlyifco-morbid
dysmenorrhoea),tranexamicacid,combinedoral
contraceptivepill
• Third-line:longactingprogestogens(oralorinjected).
ConsiderGnRHanaloguesifthisfails
Surgical:
• Endometrialablation
• Hysterectomy
• Note:Surgicalinterventioncancauseinfertility
Table3.3.Menorrhagia
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95. Gynaecology82Map3.4.Amenorrhoea
Whatisamenorrhoea?
Thismaybedefinedaseitherprimaryor
secondaryamenorrhoea:
•Primary:menstruationhasnotcommenced
bytheageof16.
•Secondary:theabsenceofmenstruationfor
6monthsinawomanwhopreviouslyhad
normalmenstruation.
Causes
Thesearesplitintoprimaryandsecondary
causes.
Primarycauses(2T2C):
•Turnersyndrome(45,X).
•Testicularfeminization.
•Congenitalmalformations(e.g.Mayer–
Rokitansky–Küster–Hausersyndrome
[Müllerianagenesis],imperforatehymen).
•Congenitaladrenalhyperplasia.
Symptoms
Dependsonthecauseofamenorrhoea.
Someexamplesarelistedbelow:
•Polycysticovarysyndrome(seeMap
3.5,p.84).
•Turnersyndrome–webbedneck,short
stature.
•Prematureovarianfailure–associatedwith
otherautoimmuneconditionssuchas
Addison’sdiseaseandhypothyroidism.
•Mayer–Rokitansky–Küster–Hauser
syndrome–varyingdegreesofuterovaginal
aplasiaorhypoplasia.
Investigations
•b-hCGlevels(urineorserum)toexclude
pregnancy.
•Bloodtests:FBC,UE,TFTs,gonadotropin
levels,prolactinlevels,androgenlevels,
oestradiol.
•Radiology:mayberequiredtovisualize
suspectedtumoursifclinicallyindicated.
MAP3.4.Amenorrhoea
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96. Gynaecology83Map3.4.Amenorrhoea
Secondarycauses(4P3H):
•Pregnancy–themostcommoncause.
•Polycysticovarysyndrome(seeMap
3.5,p.84).
•Prematureovarianfailure.
•Pituitarynecrosis–Sheehan’ssyndrome
afterPPH.
•Hyperprolactinaemia.
•Hypothalamicdisorder(e.g.anorexia
nervosa,excessiveexercise,stress).
•Hyper/Hypothyroidism.
Treatment
Dependsonthecauseofamenorrhoea.Some
examplesarelistedbelow.
Conservative:
•Patienteducation.
Medical:
•Polycysticovarysyndrome(seeMap
3.5,p.84).
•Prematureovarianfailure–hormone
replacementtherapy.
Surgical:
•Dependsonunderlyingpathology
(e.g.Mayer–Rokitansky–Küster–Hauser
syndrome–theuseofvaginaldilatorsand
surgicalproceduressuchastheVecchietti
procedure.
Complications
•Infertility.
•Osteoporosis.
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97. Gynaecology84Map3.5.Polycysticovarysyndrome(PCOS)
Whatispolycysticovarysyndrome?
Thisiswhenawomanhaspolycysticovaries.Itis
diagnosedusingtheRotherhamcriteriawheretwo
outofthethreecriterialistedbelowmustbemet:
1.Radiologicalfeatures:aUSS
visualizingmultiple(12)smallfollicles
measuring~2–9mm+/–anovarianvolume
10mL.
2.Menstrualirregularity:periodsthatare5
weeksapart.
3.Endocrinephenomena:
•Hyperandrogenism–hirsutism,acne.
Causes
TheexactcauseofPCOSisunknown.Factors
includeinsulinresistanceandhormonalimbalance
causingincreasedandrogenlevels,decreased
levelsofsexhormonebindingglobulin(SHBG),
raisedLHlevelsandsometimesraisedprolactin
levels.
Symptoms
Maybeasymptomaticbutotherfeaturesmaybe
rememberedasHAIR:
H–Hirsutism
A–Amenorrhoea
I–Irregularperiods/Increasedweight
R–Reducedfertilityandmiscarriage
Investigations
•Generalbloodtests:FBC,UE,TFTs.
•Specificbloodtests:androgenlevels,SHBG,LH,
FSH,prolactin.
•Radiology:transvaginalUSSforspecific
features(seeRotherhamcriteria).
MAP3.5.Polycysticovarysyndrome(PCOS)
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98. Gynaecology85Map3.5.Polycysticovarysyndrome(PCOS)
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Treatment
Conservative:
•Patienteducation.
•Lifestyleadvice–particularlyweightloss.
Medical:thisaimstotreatsymptoms
•Hirsutism:oralcontraceptivepillswithan
antiandrogeneffect(e.g.YasminorDianette).
•Subfertility:metforminmayhelp.
•Inducingovulation:clomifene.
Surgical:
•Notindicated.IVFmayberequiredlater.
Complications
•Infertility.
•Type2diabetesmellitus.
•Gestationaldiabetes.
•Depression.
•Increasedweight,whichleadsto
complicationssuchas:
Sleepapnoea.
Metabolicsyndrome.
Increasedriskofdiabetes.
Highbloodpressure.

99. Gynaecology86
TABLE3.4.Terminationofpregnancy(TOP).
CurrentlegalstandingMethodsusedComplications
BasedontheAbortionAct1967;amended
1990 by theHumanFertilizationandEmbryology
Act.Requiresthesignaturesoftworegistered
practitioners.FulldetailsoftheHumanFertiliza-
tion and EmbryologyActmaybefoundat:http://
www.legislation.gov.uk/ukpga/1990/37/contents
KeyfeaturesoftheAct:
• Mustbenogreaterthan24weeksgestation
• Maybeconsidered24weeksgestationifthe
lifeofthemotherisatgreatrisk
• Considerincaseswheretheremaybegreatrisk
tothemother’sexistingchildren
• Considerwhenthephysicalormentalhealthof
themotherisingreatjeopardy
• Considerifthechildishighlylikelytobeborn
withaseverementalorphysicalhandicap
ThemethodusedforTOPdependsonthegestation
ofthepregnancy.Generally,themethodsusedare
asfollows.
1. 9weeksgestation:
○ Mifepristone
○○48hoursafterdoseofmifepristone
giveprostaglandin(e.g.misoprostol).
Prostaglandinsstimulateuterinecontraction
2. 13weeksgestation:
○○Surgicaldilatationandvacuumaspiration
3. 15weeksgestation:
○○Surgicaldilatationandevacuation
Generalcomplications:
• Thoseofgeneralanaesthetic
• Haemorrhage
• Infection
• Retainedproductsofconception
• Psychiatriccomplications(e.g.depression)
Specificcomplications:
• Traumatothegenitaltract
• Asherman’ssyndrome
• Perforationofpelvicorgans(i.e.uterus,bowel
andbladder)
Table3.4.Terminationofpregnancy(TOP)
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100. Table3.4.Terminationofpregnancy(TOP)
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101. Gynaecology88Map3.6.Infertility
Whatisinfertility?
Infertilityisthefailuretoconceiveafterregular
unprotectedintercoursefor2yearsinthe
absenceofknownreproductivepathology.This
maybecategorizedasbeingeitherprimaryor
secondary.Intheformerthecouplehavenever
conceived,whereasinsecondaryinfertilitythe
couplehaspreviouslyconceived.
Fertilityrequiresanormalspermtoreacha
normaleggandthenfertilizeit.Thisfertilized
eggthenneedstoimplantsuccessfullyintothe
endometrium.Anyhindranceinthisprocess
maycauseinfertility.
Causes
Theseareclassifiedintomaleandfemale
causes.Someexamplesarelistedbelow:
•Male:occurswhenthereisaproblemwith
spermvolume,pH,concentration,morphology,
motilityorvitality.Thismaybeduetosmoking,
alcoholuse,steroidsorSTIs.
•Female:thinkofthehypothalamicovarian
axistorememberthecauses:
Hypothalamicdysfunction:
–Hyperprolactinaemia.
–Hypothalamichypogonadism.
–Hypothyroidism.
–Hyperthyroidism.
Investigations
•Semenanalysis.Normalresultsare:
Volume1.5mL.
pH7.2.
Spermconcentration15million/mL.
Morphology4%normalforms.
Motility32%progressivemotility.
Vitality58%livespermatozoa.
•Bloodtests:FBC,UE,TFTs,androgenlevels,
SHBG,LH,FSH,prolactin,21-day
progesterone(30nmol/L=ovulation).
•Radiology:transvaginalUSS,
hysterosalpingogram.
•Laparoscopyanddyetests.
Symptoms
•Primaryorsecondaryinfertility.
•Thoseofunderlyingcause.
Map3.6.Infertility
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102. Ovariandysfunction:
–PCOS.
–Prematureovarianfailure.
Tubaldysfunction:
–PID.
–Adhesionsfrompreviouspelvic
surgery.
–Cysticfibrosis.
Implantationfailure:
–Fibroids.
Anatomicalabnormality:
–Bicornateuterus.
–Mayer–Rokitansky–Küster–Hauser
syndrome.
Treatment
Dependsonthecauseofinfertility.
Conservative:
•Patienteducation.
•Regularintercourse3–4timesaweek.
•Lifestyleadvice–particularlyweightloss.
Medical:
•Clomifene.
•Gonadotropintherapy.
Surgical:
•Ovariandiathermy.
•IVF.
•Intra-uterineinsemination.
•Tubalsurgery.
Complications
•Psychologicalimplications–depressionand
anxiety.
•Sideeffectsoftreatmentsincluding:
Ovarianhyperstimulationsyndrome.
Ectopicpregnancy.
Multiplepregnancy.
GynaecologyMap3.6.Infertility89
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103. Gynaecology90
Investigations
•Generalbloodtests:FBC,UE,LFTs,TFTs.
•Specificbloodtests:colposcopywith
biopsyofcervix.
•Radiology:MRIofpelvis.
•StageusingtheFédérationInternationalede
Gynécologieetd’Obstétrique(FIGO)system.
Symptoms
•Intermenstrualbleeding.
•Post-coitalbleeding.
•Post-menopausalbleeding.
•Abnormalvaginaldischarge.
•Generalsymptomsofmalignancy(e.g.
fatigue,cachexia,weightloss).
•Asymptomatic–abnormalitiespickedupby
theNationalScreeningProgramme(NSP)UK.
TheNSPforcervicalcancerusesliquid-based
cytologytoclassifycervicalintraepithelial
neoplasiaaswellasidentifyHPVinfection.
Thisoccurs3yearlyaged25–49and5yearly
aged50–64,providingthatresultsare
normal.
Whatiscervicalcancer?
Thisisuncontrolleddifferentiationand
proliferationofcellsliningthecervix.Itmaybe
categorizedintotwodifferentcelltypes:
1.Squamouscellcarcinoma(80%).
2.Adenocarcinoma(20%).
Causes
Theexactcauseofcervicalcancerremains
unknownbutitisassociatedwithseveralrisk
factors,themostprominentbeingthehuman
papillomavirus(HPV)(seebelow).
Riskfactors
•HPV–types16,18and33.
•HIV.
•Multiplepregnancies.
•Multiplesexualpartners.
•Earlyageoffirstsexualintercourse.
•Combinedoralcontraceptivepill(COCP).
•Increasingage.
•Lowsocioeconomicstatus.
•Smoking.
Map3.7.Cervicalcancer
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