Women's and CAH OSCEs Flashcards
SX pregnancy
Nausea
Tender breasts
Missed period
Urinary frequency
Naegle’s rule
Date of conception is first day of last normal period + 9 months and 7 days
Antenatal visit frequency
> 28/40: monthly
28-36: biweekly
36: weekly
Supplements pregnant women should take
Folate
Vitamin D
Iron
Ca
Routine bloods at first antenatal visit (12 weeks)
FBE Blood group and antibody screen (ABO, Rh) HIV, HBV, HCV, syphilis Rubella immunity MSU for MCS (?asymptomatic bacteriuria)
+/- VZV immunity
+/- Down syndrome serum screen (free betaHCG, PAPP-A)
Components of combined down syndrome serum screen
12 week ultrasound - gestational age and nuchal translucency
Serum free bHCG + PAPP-A
OR as an alternative, non-invasive pre-natal screen for cell-free DNA from 9 weeks. tests for aneuploidies. 99% NPV. If pos, refer for invasive testing. Takes 3 days but costs $450.
IF a women’s combined serum screen comes back as high risk, what is the next step in investigations for diagnosis?
Refer her for diagnostic invasive testing (chorionic villus sampling at 10-13 weeks or amniocentesis at 15-18 weeks) anti-D if mum is Rh neg
+ FISH and full karyotype
when do routine USS in low-risk pregnancies typically occur.
Ultrasound @ 12 weeks: gestational age and down syndrome screen
18-20weeks: morphology and wellbeing
What bloods get done in the second trimester and when?
28 week bloods:
- FBE
- Oral glucose challenge
- AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
Who needs anti-D injections and when are these given?
Rh neg women who are negative for anti-D antibodies
Given at 28 and 36 weeks
To Rh(neg) women with M/C, invasive procedures, abruption, trauma etc
What 2 medical conditions do we screen for every visit and how do we do this?
Placental insufficiency - ask about fetal movements + SFH
Pre-Eclampsia - HTN (BP), proteinuria (urine dipstick) , oedema (exam/Hx)
What routine Inx get done in the third trimester and when?
36 weeks:
- FBE
- AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
- GBS swab! (lower vaginal and anal)
Advise to women in third trimester as to when to come to hospital
Contractions are regular and painful, occurring ~1x5min (2:10) OR:
- DFM
- Bleeding
- SROM
- Psychological distress
When does the GBS swab get done?
36 weeks, lower vaginal and anal swab
When does the oral glucose challenge test get done?
28 weeks
How do you assess fetal wellbeing antenatally (5)
- fetal movements
- maternal SFH
- USS
- Infection screen +/- karyotype (aneuploidy screen)
- CTG
Assessing fetal wellbeing in labour
- CTG
- fetal movement
- Doppler
- Fetal scalp blood sampling
what growth scan patterns do you see in IUGR babies?
GDM babies?
asymmetrically small: HC is relatively larger than AC
Asymmetrically large: AC to HC ratio high (due to glycogen deposits in liver)
Indications for elective C/S delivery for large babies
If EFW >97th centile
GDM
High AC: HC ratio (risk of shoulder dystocia)
Management of IUGR
Maternal CS administration if expected pre-term
NVD w continuous CTG monitoring if near term
If v small and v preterm, may need elective LUSCS
Maternal and fetal condition dictates need/timing of delivery
Risk factors for ovarian cancer
Protective factors
- Age
- Obesity
- Incr # ovulations (nulliparity)
- Family HX ovarian/breast/colorectal cancer:
Lynch syndrome (HNPCC) - 10% risk
BRCA1 (50% risk)
BRCA2 (20% risk) - HRT/unopposed oestrogen
Protected: OCP, multiparty, breast feeding
Clinical présentation of ovarian cancer
Bloating, abdo swelling Abdo pain Dyspepsia Urinary freq Weight change Irreg bleeding SX metastatic disease: ascites, pleural effusions, SBO/LBO
Inx for suspected ovarian cancer
TVUSS
Bloods: CA125 and CEA ; hcG, LDH, alpha fetoprotein
Risk factors uterine cancer
- Age
- Caucasian
- nulliparity
- early menarche, late menopause
- Hx infertility
- HRT/tamoxifen
- Obesity
- Diabetes
- PCOS
- Endometrial hyperplasia
- HNPCC
- Endometrial polyps
Presentation of cervical cancer
Early stage:
Asymptomatic
Post-coital bleeding, AUB, PMB, vaginal D/C
Late stage:
- pelvic or back pain
- Sciatica/neuropathy
- enlarged groin nodes
- bladder/bowel SX, lower limb oedema
Risk factors for cervical cancer
SMOKING Long term OCP use HIV, immune suppression High parity Chlamydia trachoma's, HSV infection Uncircumcised male partner
What can HPV virus cause?
Genital warts (warts elsewhere too, like plantar warts etc) Cervical cancer Vulval/vaginal cancer Anal cancer Penile cancer
Natural history of HPV infection of cervix
Normal cervix HPV infected cervix with mild-cytological abnormalities. This can be cleared by the immune system so the cervix goes back to normal, or can progress to a precancerous lesion (CIN 1 and 2 which are LGSIL or CIN3 which is HGSIL). Most LGSIL regress without treatment.
Most HGSIL will progress over 7-10 years, if not treated, to invasive cancer (carcinoma in situ)
When is the guardasil vaccine given and what HPV strains does it protect against?
Given at 0, 2, 6 months of age
HPV 16,18,11
Management of LGSIL found on pap test
Mostly acute/transient HPV infection that the body clears within 12 months
NO TREATMENT. Repeat smear yearly until 2 consecutive neg results, then return to normal bi-yearly screening.
If a second LGSIL -> colposcopy and biopsy -> if confirmed normal or LGSIL, screen again in 12 months; if confirmed HGSIL, treat.
If any progression to HGSIL on repeat smears, straight to colposcopy and biopsy
Management of HGSIL found on pap
Colposcopy and biopsy
Confirmation on biopsy needs tx:
Conservative
- LLETZ (most common tx mode) = large loop excision of transformation zone
- Cone biopsy (only used for adenocarcinoma in situ due to incr risk profile)
Definitive
- Hysterectomy (fertility not desired)
How might an ovarian germ cell tumour present?
Non specific abdo sx
- abdo distension and pain (? ruptured cyst or torsion)
- mass effects (bladder, bowel sx)
- Menstrual irregularities
- SX of pregnancy
- SX of metastatic disease (ascites, lymphadenopathy)
How does GTD present?
Usually presents as miscarriage <10weeks and is diagnosed on post-mortem histopath
Sx of pregnancy
Early pregnancy PV bleeding
irregular vaginal bleeding
What hormone does GTD produce and how is this helpful clinically?
produces hCG, used as a tumour marker for diagnosis (serial hCG) and follow-up/monitoring
Which type of benign molar pregnancy has a higher risk of progression to neoplasia?
Complete
When does GBS sepsis present and what are risk factors for the congenital infection?
First 24 hours of life
RF: premature, PROM >18 hours, maternal fever, GBS positive mother (carries it in her GI/GU tract)
MX of a GBS positive mother
IV intrapartum antibiotics: 2 doses 4 hours apart, starting at onset of labour (IV benpen or cephazolin if allergic)
Neonatal obs for 24 hours following delivery +/- neonatal abx if clinical suspicion of sepsis
Consequences of maternal parvovirus B19 infection in pregnancy
If primary infection in pregnancy, small risk (3-5% of maternal infections) of fetal hydrous and intrauterine death secondary to fetal anaemia
Risk factors for chorioamniotis
PROM
Prolonged labour
Multiple intrapartum VEs
Internal fetal HR monitoring (scalp electrode)
Genital tract infections (STIs, GBS positive)
Clinical features of chorioamnionitis
Maternal fever or fetal tachycardia Uterine pain/tenderness PV blood loss Preterm labour Malodorous or purulent amniotic fluid FBE: Incr WCC + incr CRP
Management of chorioamnionitis
Erythromycin for 10 days + steroids
Immediate delivery if baby is unstable (even if preterm, if infected - i.e. baby tachycardia, offensive D/C, pain, bleeding)
Pathophys of menopause
how do hormones change with this?
Physiological - loss of ovarian function from exhaustion of primordial follicles due to atresia/atrophy
Iatrogenic - gynae surgery (bilateral oophorectomy; chemo, radiation to pelvis)
Decr Estrogen and progesterone
Incr FSH
Symptoms of menopause and what do they relate to?
SX Related to decr oestrogen
Vasomotor SX (hot flushes, night sweats, palpitations)
Sleep problems
Urogenital problems (dry vaginal, atrophic vaginitis, urinary frequency)
Locomotor sx (joint pain, backache, muscle aches)
Psychological SX (anxiety, depression, feeling unloved etc)
Loss of libido
Osteoporosis and incr fracture risk
Management of osteoporosis in menopause
All women with risk factors get 2 yearly DEXA scans
T-scores <2.5 get treatment:
Lifestyle/conservative: Ca, vit D supplements and daily exercise
<60: HRT
>60: Bisphosphonates (SE: GORD, osteonecrosis of the jaw)
Risk factors for osteoporosis
Low BMI (decr fat - decr oestrogen which is protective) Smoking Family Hx excessive caffeine steroids IBD/malabsorption Decr VitD
Definition of menopause
normal age range
final menstrual period, determined after 12 months of amenorrhoea
normal age range: 45-57
Non-hormonal management of menopause
Lifestyle:
- stop smoking
- weight mx (exercise and diet)
- <2SD alcohol
- Decr caffeine
SX-treatment Vasomotor SX - SNRI (Venlafaxine, fluoxetine, citalopram) - GABApentin - Clonidine/nifedipine (Ca ch blocker)
Vaginal dryness
- vaginal oestrogen pessary
- lubricants and gels, moisturisers and oils
Locomotor SX: analgesia, NSAIDs, exercise
Psych SX: Antidepressants, anxiolytics, counselling
Hormonal management of menopause
- HRT (only for women <60 to limit risks of CVD, VTE, stoke etc)
Relieves menopausal SX and incr bone density
With uterus: Oestrogen and progesterone (protects from incr risk of endometrial cancer)
Method: local cream/pessary/tablet if vaginal dryness (no need for prog)
- tablets, patches, subcut implant, skin gel (combined preparations)
Without uterus: oestrogen alone
- Tibolone: synthetic steroid with weak oestrogen, progesterone and anti androgen effects (helps w vasomotor SX, vaginal lubrication and libido; incr bone mass density and decr fracture risk; no incr risk endometrial cancer)
SE of HRT and CI
SE:
incr risk stroke, VTE, CVD (oestrogen)
incr risk breast cancer (combined - prog)
incr risk endometrial, ovarian cancer and cholecystitis w unopposed estrogen
CI: HX breast, ovarian, endometrial cancer HX VTE or thrombophilia HX stroke or heart disease Uncontrolled HTN Active liver or cholestatic disease Migraine w aura Abnormal vaginal bleeding
Investigations for premature menopause (<45)
FSH (elected on 2 occasions is diagnostic)
Decr E2
Inx for other causes
prolactin, TFTs, betaHCG
Karyotype (turner’s) and fragile X screen
pelvic USS
Differentials deep dyspaerunia
Endometriosis Adenomyosis Adhesions PID Fibroid Neoplasia
Differentials superficial dyspareunia
Vulvovaginitis (inflammation) - thrush, STIs, herpes, UTI
Dermatological - lichen sclerosis, eczema, psoriasis, contact dermatitis, atrophic vaginitis
Inadequate lubrication - menopause, oestrogen deficiency, radio/chemotherapy, drugs
Trauma
Vaginismus (spasm of vaginal muscles)
Vulvodynia
Rigid hymen
Neoplasia
Aetiology post-menopausal bleeding
Anovulatory cycles (lack of ovulation leads to endometrial build up that outgrows blood supply)
Cervical:
Cervical cancer (70% SCC due to HPV; 30% adenocarcinoma)
Cervical polyps
Cervicitis
Endometrial:
- Endometrial cancer until proven otherwise
- Endometrial atrophy (due to lack of oestrogen, thinning of vaginal and cervical epithelium and endometrium)
- Endometrial polyps
- Fibroids
- Endometrial hyperplasia (simple; atypical - 40% progress to carcinoma)
- Endometritis/PID
Vaginal - thrush, atrophy, cancer
Trauma
Inx and Mx of post-menopausal bleeding
Inx: TVUSS and hysteroscopy DandC or O/P pipelle for endometrial sampling (colposcopy if pap spec and pap smear abnormal)
MX:
Medical
- vaginal oestrogen therapy for urogenital atrophy
- Progesterones (mirena, depot provera injections) for SIMPLE endometrial hyperplasia
- COCP if <60 and low risk for CVD, VTE
Surgical
- Hysterectomy for atypical endometrial hyperplasia (+/- bilateral sapling-oophrectomy with lymph node sampling for endometrial cancer; +/- pelvic lymph node sampling for cervical cancer)
- Endometrial ablation + contraception or tubal ligation
Vaccines given at birth
HBV
Vaccines given at 2,4,6mo
DTPa (Diptheria, tetanus, whooping cough)
HIB
IPV (inactive polio vaccine)
HBV
PCV (13v pneumococcal conjucate)
RV (Rotavirus)
Vaccines given at 12mo
MMR (measles, mumps, rubella)
HIB
MenCCV
Vaccines given at 18mo
VZV (chickenpox)
MMR (measles mumps rubella)
DTP
Vaccines given at 4y
DTPa (diphtheria, tetanus, pertussis)
Polio
Vaccines given at 10-15y
DTPa (diphtheria, tetanus, pertussis)
VZV (chickenpox #2)
HPV
Side effects of vaccines
- Local superficial inflammatory response -> redness, swelling at injection site
- Mild transient systemic SX (crying, irritability, mild fever, febrile seizures)
- Measles may be followed by mild, transient measles like illness (fever and brief rash 7-10s post immunisation)
Rare:
Anaphylaxis
Seizure
Contraindications to vaccines
Unexplained encephalopathy after a previous vaccine
Anaphylaxis after a previous dose
Immunodeficiency - for live vaccines (eg Rotavirus, MMR, Varicella)
Relative CI:
- Evolving (undiagnosed) neurological illness
- Fever >38.5
Gross motor milestones
Head lag minimal at 6-8 weeks
Rolling at 3-5 mo
Sitting at 6 months
Crawling at 9 mo
Walking at 12 mo
Jumps BY 3 years
Balances on one foot BY 4.5 years
Red flags for gross motor milestone
Not walking by 18mo
Fine motor milestones
Palmar grasp by 6mo
Inferior pincer by 9mo
Pincer grip, stacks 2 cubes ~ 12mo
Handedness 18mo
Spontaneous scribbling by 2years
Imitates vertical line by 3 years
Copies face/ladder by 4.5 years
Social and daily living skills milestone red flags
No interest in other children/help w dressing at 24 months
NO interactive play with peers at 3 years
No imaginative role play by 4 years
Language milestones
3mo - coo 6 mo - babble 9mo - mamma danda 12mo - 3 words 18mo - understands nounds 2y - 2 step command; 50 words 3t - understands negatives 4yr - 3 stage command; knows relative adjectives
Social milestones
3mo - simle
6mo - mouthing
9mo - stranger anxiety and holds and bites food
12mo - clap
2 yrs - eat w spoon
3ys - share play
4 yr - concern and sympathy; imaginative play
DDX vomiting in 6mo year old
Overfeeding
GORD
Malrotation
Pyloric stenosis
Intussusception
Sepsis (lungs, UTI, GE)
features of malrotation
Early signs
- Bilious vomiting (flour green)
- Poor feeding
Late signs include: PR bleeding, abdominal distention and tenderness
What causes malrotation?
Anatomical variation where base of mesentery is narrow which means DJ flexure and Ileocaecal flexure are next to each other, in RUQ which results in SHORT BASE OF MESENTERY and predisposes the mesentery to volvulus
How do you diagnose malrotation?
What is the treatment?
Upper GI contrast study is gold standard - look for LOSS OF C-shaped duodenum to indicate malrotation
Or AXR changes: double bubble, gastric and proximal duodenal dilatation…
Urgent surgical referral and laparotomy -> LAdd’s procedure + appendicectomy
When does malrotaiton w volvulus generally present?
50-75% within 1st month of life
90% within a year of life
Typical presentation of hypertrophic pyloric stenosis
PYLORIC STENSOSIS: Typically first born boys, with non-bilious projectile vomiting (vomit past their feet) after each feed who are HUNGRY after!
- family history of HPS
- visible gastric peristalsis
+/- palpable pyloric tumour (‘olive’) if stomach isn’t too distended
When does pyloric stenosis typically present?
Peak 3-6 weeks old
But can occur 10 days-11 weeks
What metabolic derangements do you see in pyloric stenosis and why?
Due to profuse vomiting -> losing water, HCL, NACL, K
Metabolic alkalosis
Hypochloraemia
Hypokalaemia
Normal serum na
Acidic urine (paradoxical change - kidneys conserve Na as compensation)
What is intussception and what generally causes it?
Invagination of proximal into distal bowel
- Peaks at 5-11 months
- Physiological/idiopathic cause is most common (hypothesised that as babies wean, new antigen exposure causes payer’s patches in terminal ileum to swell from inflammation and cause intussception)
Less commonly can be due to pathological lead points
Classic presentation of intussception
Crampy (intermittent, also known as colicky) Abdominal pain (infant pulls legs into stomach to relax abdo wall)
Vomiting
Diarrhoea at first, then maybe constipation
Bloody ‘red currant jelly’ stools (LATE sign)
Sausage shaped mass in RUQ and emptiness in RLQ.
Complications of intussception if not treated early
BO
Ishcaemia, Perf, shock
How do you diagnose intussception?
Clinical suspicion -> US (‘target sign’) is first choice
or AXR (?soft tissue mass ?absence of gas in caecal region)
Tx intussusception
<48 hour history in otherwise stable child = air enema reduction
> 48 history or peritonitic/septic child = laparotomy
Treatment pyloric stenosis
Fluid rehydration therapy and electrolyte replacement
- 0.45% saline with 5% dextrose
- Add K when baby is urinating
Non-urgent surgical referral
DDX for acute scrotum (red, painful, tender scrotum)
Immediate management
- testicular torsion
- torsion of appendix testies
- epididymo orchitis
- idiopathic scrotal oedema
Urgent surgical referral ?surgical exploration
Classic presentation of appendicitis
Colicky periumbilical pain migrating to RLQ and becoming constant
Assoc w :
- anorexia
- fever
- nausea
- d&v
Classifying seizures
GENERAL seizure - always involve consciousness AND motor manifestations!
(tonic clonic, myoclonic, atonic etc)
PARTIAL seizure
- Simple partial seizure: consciousness intact (motor, somatosensory, visual/auditoary, autonomic, dysphasic)
-Complex partial seizure
(consciousness not intact)
2 year old with incomplete immunisations at creche with fever and cough, coryza, conjunctivitis progressing to descending, blotchy raised (papular) rash
- diagnosis
Measles
Things that incr change of fit in epilepsy
Stress
Fatigue/lack of sleep
Alcohol
COMPLIANCE
DDX for generalised tonic clonic seizure (and what you would expect for each on history)
COMMON
- Febrile seizure - in context of fever and infection (UTRI, UTI)
- Breath holding
- vasovagal syncope
REDFLAG
- Metabolic - DKA or hypoglycaemia
- HEAD trauma -> intracerebral pathology
- Sepsis/meningitis
Focal seizure becoming generalised
□ Preceding aura (note: NO aura with generalised TC)
□ Todd’s paresis (transient unilateral postictal weakness)
□ Focal neurological deficits on exam
□ HX of prior CNS illness/cerebral trauma
Psychogenic seizure
□ Eye closure during seizure
□ Resistance to passive eye opening
□ Intermittent or waxing and waning motor activity
Upper limit of normal for axillary temp
Axillary > 37.2C
What do you do if a child comes in with a fever?
If child is : > 3months non toxic fever <14 days It is likely viral so DON'T do septic screen (possibly check urine ex: if <6 months) and review to ensure they don't deteriorate.
Otherwise they get a septic screen
What comprises a septic screen?
FBE, blood film
Blood and urine cultures
LP +/- CXR (if resp SX/signs)
What questions to ask on HX when a child comes in with fever
Localising symptoms: cough coryza headache photophobia diarrhoea, vomiting abdominal pain joint symptoms
Travel history
Sick contacts
Immunisation hx
Presentation of meningococcus
Rapid onset
Fever
Flu-like SX (malaise, lethargy, vomiting, headache, myalgia, arthralgia)
Confusion
Rash (petechial/purpura)
Photophobia
Neck pain/stiffness
Differentials for child presenting with fever and petechial rash (previously well, onset this am)
Meningococcus if unwell/shocked/toxic
Viral infection (enterovirus, influenza)
HSP
ITP
15 month old presents with a non-itchy blanching erythematous rash (not on face) following 3 days of sudden-onset high-grade fever and a single febrile seizure.
What’s your top differential? Treatment?
HHV6 (roseola)
No treatment required - self limiting.
Child presents with ‘slapped cheek’ rash on face and lacy rash on trunk and limbs following low-grade fever, malaise, or a “cold” a few days before the rash broke out.
Differential? Treatment? Complications?
Parvovirus B19
No treatment required bc is viral
+/- Paracetamol to bring down fever
If exposed to ParvovirusB19 in first half of pregnancy, baby can get fetal aplastic anaemia hydrops fetalis and fetal death (miscarriage)
Occurs in 5% of pregnant women infected with parvovirus
What are the clinical features of measles?
4 day infectious prodrome (3 Cs) preceding rash:
Cough, coryza, conjunctivitis
Fever
Koplik’s spots
Rash (red, blotchy, DESCending - starts on the head and then spreads to the rest of the body) - lasts ~7d
Management for measles
Supportive - fluids, panadol
MMR vaccine (2 doses) within 72 hours of exposure if >9mo
IVIG if <9mo or >9mo but >72 hours post exposure
Differentials for diffuse erythematous rash (sunburn-like) in child
Bacterial:
Toxic shock syndrome (Staph or strep)
Scarlet fever/Invasive GAS
Viral
Other:
Kawasaki disease
Antibiotics
What causes Scarlet fever?
Exotoxins from Group A Strep (pyogenies)
Clinical presentation of scarlet fever
Exudative tonsillitis +/- pharyngitis Confluent erythematous sunburn-like rash Strawberry tongue Circumoral pallor lymphadenopathy fever
Treatment of scarlet fever
Penicillin (oral) - to treat GAS
Features of Kawasaki disease
CRASH&BURN
Conjunctivitis - Bilateral non-exudative
Rash - polymorphous
Adenopathy - Unilateral cervical >1cm
Strawberry tongue/Mucus membrane changes (oropharynx injected, swollen lips)
Hands - Swollen erythematous hands and feet with eventual desquamation
BURN - Fever>5 days (unresponsive to antibiotics)
Treatment of kawasaki disease
IVIG and low-dose aspirin
Complication of kawasaki disease
Coronary artery aneurysm
Higher risk of IHD
Features of infectious mononucleosis (glandular)
FEVER Exudative pharyngitis Tonsillitis Lymphadenopathy Splenomegaly Palatal petechiae Rash
Tx mono
None
Steroids only if airway obstructed due to tonsillar enlargement
Signs of resp distress in a newborn
○ Tachypnoea (>60breaths/min)
§ In response to incr CO2 in order to breathe out and decr the CO2
○ Expiratory grunt
§ Produced by exhalation against a partially closed glottis in order to increase PEEP and therefore keep alveoli open
§ May be interpreted as crying or moaning
○ Recession of intercostal spaces and suprasternum; in drawing of subcostal margin
§ Due to the increased resp effort generating more negative intrapleural pressure which sucks in the softer/more compliant chest wall during inspiration
○ Nasal flare
§ Flare during inspiration decreases airway resistance
○ Central cyanosis
§ Note - polycythaemic babies will appear cyanosed at relatively high O2 sats but babies with low Hb will not appear cyanosed until saO2 is v low.
○ Deranged temperature control
○ Low O2 saturation
What is TTN?
RF?
Tachypnoea of the newborn (TTN) = wet lung
retention of fetal long fluid
□ C-section without labour -> ‘Cold’ c-section = no maternal hormone surge hasn’t caused resorption of fluid yet
□ Breech delivery
□ Male sex
□ Birth asphyxiation
□ Heavy maternal analgesia
Mx TTN
most babies settle in 24-48 hours with minimal handling and cot O2.
CPAP if acidotic, low sats, working hard to breathe.
What is infant RDS? Another name for it?
Who gets it (1 RF)?
Treatment?
= hyaline membrane disease
§ Occurs in pre-term infants due to surfactant deficiency in the alveoli
Mx:
Empirical abx because looks similar to sepsis!
CPAP
If need more, intubate and give surfactant (need intubation).
Characteristic CXR appearance of RDS/HMD
Hypo aeration, diffuse GROUND GLASS appearance, air bronchograms
RF mec aspiration
Post-term (>40 weeks)
Births involving fetal distress
RF for neonate sepsis
Maternal GBS positive
Maternal fever
Prolonged rupture of membrane (>=18 hours)
Abx coverage for neonatal sepsis (what bugs are you worried about?)
Gentamicin (listeria, e coli, HIB)
Benzyl-penicillin (GBS)
Differentials for resp distress
Apnoea of prematurity TTN/wet lung HMD/RDS Meconium aspiration syndrome Sepsis Pneumothorax Cardiac (VSD, PDA, transposition, pulm HTN) Congenital pneumonia NEC/bowel obstruction Congenital diaphragmatic hernia Anatomical - although not usually in neonatal period (laryngomalacia etc) Severe anaemia/fetal hydrops Maternal GDM Drugs ?
complications of genital prolapse
Hydronephrosis (obstruction of ureters in severe cases)
Urinary retention (outflow obstruction)
Faecal incontinence
Rectal prolapse
Haemmharoids
SX of genital prolapse to ask about
Dragging/heavy sensation in vagina Lump/bulge in vagina Difficulty emptying bladder/bowels Difficulty inserting tampons Urinary/fecal incontinence Haemmharoids lower back pain DC/bleeding from ulceration
Management of genital prolapse
Reassurance
Reversible risk factor identification and lifestyle changes (weight loss, stop smoking, constipation)
Pelvic floor exercises - liase w physio and continence nurse
Vaginal oestrogen supplements (topical creams)
Vaginal pessaries!
Surgery last line
How do you assess the progress of a woman in labour?
- Abdo palpation hourly
- Contractions - duration, freq, intensity
- VE - 4 hourly (as long as membranes are NOT ruptured)
Options for intrapartum pain relief
Support person
NO mask
PCA Narcotics (morphine has longer half life than fentanyl or pethidine)
Regional anaesthesia using lignocaine or bupivicaine (epidural for labour ward; spinal for theatre, faster onset action but shorter t1/2)
What defines Hyperemesis gravidarum. What complications do you have to watch for?
Excessive pregnancy related vomiting and nausea that prevents adequate food and fluid intake and is assoc w >5% LOW, usually peaking mid-first trimester
Complications: dehydration, malnutrition, electrolyte imbalance, mallory-weiss tear with prolonged/severe vomiting, hyperthyroid (due to cross-reactivity between TSH and HCG)
RF for hyperemesis gravidarum
Previous HG Multi-pregnancy Molar pregnancy Female embryos Increase free beta HCG (molar pregnancies)
Investigations for vomiting in pregnancy and why (ddx to consider)
UEC, LFTs, TFTs, FBE +/- CRP
urine MCS and dipstick
Exclude UTI, gastro/other infection, biliary disease, appendicitis, Addison’s disease, Thyroid disease, electrolyte disturbances from extreme dehydration
What is pre-eclampsia?
De novo HTN (>140/90, or >30/50 over baseline) arising after 20/40 and returning to normal within 3 months postpartum + evidence of dysfunction in at least one other organ (kidney, liver, neuro, haem, fetus)
RF for Pre eclampsia
First pregnancy or new paternity Age extremes (teens and >40) Obesity Smoking Previous PE Family HX Assisted reproduction
Medical conditions: essential HTN, GDM, RA, SLE, renal disease etc
Large placenta - Multi pregnancies, GDM, GTD
Clinical features of Pre Eclampsia
Stage 1: isolated HTN
Stage 2: + Proteinuria + Generalised swelling (facial and lower limb)
Stage 3 = Eclampsia
Signs of multi system dysfunction…
- Neuro: SEIZURES!! Headaches +/- visual changes; hyper-reflexia and/or clonus
- Renal: Oliguria, renal failure
- Hepatic dysfunction: Epigastric/RUQ pain/lower abdo pain
- CV: CCF, Pulm oedema (SOB)
- Haem: thrombocytopenia, haemolysis, DIC
- Uteroplacental: decr FM, IUGR, abruption, FDIU
Investigations for Pre Eclampsia
FBE (plt, Hb)
UEC (renal function and uric acid)
LFTs (ALT deranged w liver dysfunction)
24 hour urine collection or spot Cr:urea ratio
CTG and USS (assess growth, AF, UA)
Definition of Eclampsia
Seizures assoc w PE due to hypo perfusion of brain
Prevention of Pre Eclampsia.
Which women should get this?
Low-dose Aspirin and Ca supplements in high risk women
High dose folate
Diet (antioxidants, Mg, zinc, fish oil), exercise, bed rest
Salt restriction
+/- LMWH for women with genetic/acquired thrombophilias
High risk: HTN, renal disease, obesity, insulin resistance, GDM, assisted reproduction, and a history of preeclampsia in a previous pregnancy,
Treatment of VTE in pregnancy
LMWH for 6 weeks post part and for remaining duration of pregnancy
Can change to warfarin postpartum
+ needs LMWH throughout next pregnancy up to 6 weeks postpartum for prevention
Clin presentation GDM
Asymptomatic, picked up on routine 28 week GTT
SX of hyperglycaemia (polyuria, polydipsia)
Incr SFH
MX of GDM
Multidisciplinary care
1. Education. Diabetic education nurse, dietician, endocrinologist, obs/gynae input
- Frequent self monitoring of capillary BSL (fasting <5mmol, 1hr post prandial <8mmol)
- Diet and exercise daily
- Add insulin and/or sulfonyelurea/metformin if targets not met - Antenatal Fetal monitoring
- Additional routine growth scans
- Regular clinical assessments of growth (SFH) - Consider IOL/electice LUSCUS after 38 weeks if poorly controlled /evidence of fetal involvement
- Close fetal monitoring intrapartum
- Postpartum neonatal follow-up monitoring for jaundice, RDS, hypoglycaemia, hypocalcaemia
- Screening GCT early in future pregnancies
Consequences of GDM
Fetal
- Macrosomia
- Shoulder dystocia
- Birth Trauma (fractures)
- Birth asphyxia
- Polyhydramnios (polyuria)
- Congenital abnormalities
- Stillbirth
Maternal
- HTN disorders
- Infection
- Caesarian/instrumental delivery
- ?PPH and Perineal trauma
- 50% incr lifetime risk of developing T2DM
Neonatal:
- hypoglycaemia
- hypocalcaemia
- RDS
- jaundice
- NICU/SCN admission
- perinatal mortality and morbidity (incr risk obesity, DM)
What is the definition of a miscarriage?
When is the risk of this highest?
SX?
Spontaneous loss of pregnancy <20weeks gestation
Highest risk <12/40
SX: lower abdo pain + PV bleeding
Definition of recurrent miscarriage.
What investigations would you perform?
> 3 consecutive miscarriages
Advice after a M/C
Pain and bleeding similar to a period is normal for ~2 weeks, treat w over the counter analgesia
Strong pain/heavy bleeding/abnormal DC/fever -> see doctor or ED
Avoid sex until bleeding stops, pain lessens
Use pads, NOT tampons until bleeding stops
Need anti-D injection if Rh(D)neg and Ab neg.
Wait until after next normal pregnant to try getting pregnant again (slightly incr risk of m/C again if you get pregnant within 4-6 weeks)
Risk factors for ectopics
STIs Smoking Prior ectopic Incr age Prior tubal surgery/ligation IVF Progestogens Contraceptive failures (pregnant with IUD)
Presentation of ectopic pregnancy
Pelvic pain (unilateral or generalised)
Delayed period
Early pregnancy abnormal bleeding
Pallor, hypotension, tachycardia, guarding/peritonism indicate ruptured ectopic -> shock
On exam: PV bleeding, closed cervix, adnexal mass, Localised tenderness
Inx for suspected ectopic
TVUSS (free fluid, adnexal or fallopian tube mass, absence of IU gestational sac)
Serial betaHCG high (>1000) but rising less than 60% over 48 hours
FBE, blood group and cross match
MX of ectopic
If in shock: emergency laparotomy
Not in shock:
- If HCG<1000: Admit for Observation, await natural resolution (betaHCG and USS monitoring)
- If HCG>1000 or keeps rising:
Medical (for small tubal ectopics and minimal bleeding): Methotrexate IM
Surgical (for large ectopics or IU bleeding): laparoscopy and salpingectomy/salpingostomy
Follow up: serum B-HCG on days 4 and 7, should decr to ensure complete removal
Psych support
Impact of ectopic on future pregnancies
Incr risk of future ectopic so future pregnancies require early TVUSS at 5-6 weeks to ensure they are intra-uterine
Take folate when trying to get pregnant in future.
Wait 2 months post surgery and 4 months post medication to try for another baby
CI to the COCP
Women with IHD Previous stroke, VTE Breast cancer Severe liver/biliary disease Breast feeding with infants <6mo Migraine with aura
What happens if you miss one COCP pill?
What happens if you miss 2 or more?
1 missed pill: take it as soon as you remember
2+ missed pills: take the last missed pill as soon as you remember even if it means taking 2 on one day. Don’t worry about other missed pills. Then use condoms/abstinence in conjunction with active pills for another 7 days, even if this means skipping the placebo pills and running 2 packs together.
Mechanism of action of the COCP
Progesterone
- prevents LH surge which prevents ovulation
- thickens the cervical mucus impeding sperm passage
- thins endometrium making it less favourable for implantation
- decr motility within fallopian tubes
Oestrogen
- stabilises endometrium to reduce irreg bleeding
- prevents follicular maturation
Advice for starting the COCP
Start on days 1-5 of menstrual cycle (period) and you will be protected immediately, OR use back-up contraception until you have taken 7 active pills
You can start at any time if you are SURE you aren’t pregnant (abstinent etc)
Risks vs benefits of the COCP
Benefits:
- reversible contraception
- decr PMS SX, can help w acne and PCOS
- decr painful/heavy bleeding
- predictable, regular bleeding
- controls vasomotor SX around menopause
- reduces risk of endometrial and ovarian cancers
Risks:
- hormonal SE
- user dependent
- incr risk VTE, stroke, breast cancer, CVD, cholecystitis
Which women is the progesterone only mini pill good for?
Breast feeding women (COCP CI for babies <6mo)
Women in whom oestrogen is CI (breast cancer, risk of VTE etc)
How does the mini pill work?
SE
Continuous release of low dose progesterone keeps the lining thin and thickens cervical mucus, can also prevent ovulation.
SE - unpredictable bleeding and spotting because there are no scheduled withdrawal bleeds.
How does the nuva ring work?
Soft vinyl ring placed in vagina that releases constant dose of oestrogen and progesterone to vessels underlying vaginal skin
Stays in place 3 weeks then is removed for a week, in which a withdrawal bleed occurs. Put a new one in after that.
How does Depot Provera work?
Adv and disadv?
Injectable (IM) progesterone-only contraceptive lasting 3 months.
Adv: only need it 4x year; can lighten periods (not in everyone though)
Disadv: Irregular bleeding/spotting, irreversible, delay in return of ovulation after sensation by ~8mo, weight gain, not for long-term use due to risk of osteopenia/osteoporosis with lack of oestrogen
What is implanon and it’s advantages and disadvantages
Rod-implant that releases progesterone
Adv: Efficacy ~99.9%, no decr in bone density, is immediately reversible, not user dependent
Disadv: Intermittent bleeding and hormonal SEs
How does the copper IUD work and what are side effects
Cu is toxic to sperm
Acts as a IU foreign body which interferes with implantation
Lasts 10 years or 5 years
SE: incr bleeding and pain with periods after insertion
Expulsion, perforation, infection, bleeding, pain on insertion
How does the progesterone IUD work and what are advantages and disadvantages?
Delivers progesterone to uterus at constant rate, thickens cervical mucus and thins endometrium
Adv: minimal systemic SEs, 90% women report lighter or no periods after 6 months
lasts 5 years, cheap
Disadv: risk of perf, infection, pain, bleeding, expulsion, vasovagal on/soon after insertion
Incr relative risk of ectopic or miscarriage if you get pregnant with it in situ (but 99.7% protection)
Advice on natural family planning
Most fertile from day 8-19 inclusive (5 days either side of day 14) so avoid unprotected sex on these days to avoid getting pregnant (only reliable in women w regular cycles)
- Thin fertile mucus and 0.3C rise in temp during ovulation are other indicators
- only 75% accurate
GI physiological changes in pregnancy
GORD due to relaxation of smooth muscle sphincter by progesterone, and incr IAP
Incr aspiration risk under anaesthesia
Haemmharoids due to incr IAP
Constipation due to smooth muscle relaxation by progesterone
Gallstones (decr gallbladder motility)
DDX genital itch (females)
Infection
- candida albicans
- Bacterial vaginosis
- Trichomonas vaginosis
- Genital warts
- Pinworms (night time itch)
- Pubic lice
Inflammation
- irritant contact dermatitis
- lichen sclerosis
- psoriasis
- allergic dermatitis
- allergic urticaria
Neoplasm
- VIN
- vulval cancer (SCC)
Atrophic vaginitis in post-menopausal women or women who are breastfeeding (decr levels oestrogen)
What is bacterial vaginosis?
SX
Diagnosis
Tx
Disturbance of normal bacterial equilibrium in the vagina - overgrowth of anaerobic bacteria
SX: abnormal vaginal discharge (alkaline white-grey discharge with fishy odour) + EXTREME ITCH in women of reproductive age
DX: high vaginal swab -> microscopy and culture
Tx: oral metronidazole; topical in pregnant women to reduce systemic side effects.
How does trichmononas vaginalis present?
What sort of bug is it?
How do you diagnose it?
How do you treat it?
Males - asymptomatic
Females - malodorous vaginal (frothy yellow-green fishy) discharge + ITCH
Protozoan parasite
Dx: high vaginal swab for microscopy and culture
Tx: oral metronidazole
Chlamydia Trachomatis:
SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?
SX: Males - urethritis
females - asymptomatic but may get vaginal d/c, dysuria, dyspareunia, post-coital bleed
Long-term can result in PID, ectopic, infertility, pain
Bacteria
DX: endocervical swab (women) or urine (males) for PCR
tx: single dose azithromycin OR doxycycline 7 days bd + test for cure 2-3 months post-treatment
Gonorrhoea
SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?
SX: males are 75% asymptomatic
females - dyspareunia, irregular bleeding, abnormal discharge, bartholin’s abscess, infertility/ectopic, chronic pelvic pain (but can be asymptomatic)
Bacteria
DX: endocervical swab for PCR and MCS
Tx: single dose IM ceftriaxone
What HPV strains cause genital warts?
6 and 11
Candida albicans
SX
DX
TX
Cottage cheese DC + itchy, irritated vulva
RF: immunosuppression, diabetes, pregnancy, use of broad-spectrum abx or exogenous steroids
High vaginal swab for MCS
Tx - fluconazole for 1 week
HSV
SX
How do you diagnose it?
How do you treat it?
type 1 causes oral lesions and type 2 causes genital ulcers
Tiny punched out extremely painful ulcers with discharge
Primary episode is severe +/- flu-like illness, with recurrent episodes more mild
Dx- swab lesions for viral PCR, and serology (IgM and IgG)
MX - acyclovir within 2-3 days of sx onset, especially in third trimester of pregnancy (+ LUSCS)
+/- topical lignocaine for pain
DDX constipation in kids
Functional - most common!
Organic
- Cow’s milk allergy
- Coeliac disease
- Hypothyroid
- HyperCa
- Meds (opiates, antichol)
Neonates
- Hirschsprung’s
- Pyloric stenosis, malrotation +/- volvulus, incarcerated - inguinal hernia
- Meconium ileus (CF)
- CP
- SC or neurol problems
- Anatomical malformations (imperf anus, duodenal atresia - both often assoc w down’s syndrome)
Causes of delayed passage of meconium
Cystic fibrosis Malrotation +/- volvululus Fistula Imperforate anus Down Syndrome Hirschsprung's
Functional causes of constipation in kids
- withholding behaviour
- pain
- anxiety
- diet
- dehydration
- change in lifestyle (weaning onto solids, toilet training, starting school)
Mx constipation in kids
- Change behaviour (toilet sits, position on toilet, stool diary)
- Diet - incr fluid and fibre, healthy diet
- Education
- Disimpaction if there is significant impaction that they are unlikely to pass (movicol adult doses as OP or colonlytely as IP)
- Laxatives
Regular review and monitoring
Laxative medications used in children
Paraffin oil (softener)
and/or
Movivol or osmolax (osmotic laxatives)
Laxative medications used in infants and neonates
Coloxyl drops (stool softener)
DDX vomiting - older kids
Migraine headache Intracranial neoplasm (morning vomiting and headaches) Acute appendicitis and peritonitis (>5yo) Poisoning Psychological (anxiety, stress) Sepsis Meningitis/encephalitis Pregnancy
DDX vomiting neonates
Systemic infx/sepsis
UTI/renal disease
Bowel obstruction (anal atresia, duodenal atresia, Hirschsprung, meconium ileus w CF, incarcerated inguinal hernia)
Malrotation +/- volvulus
Hypoglycaemia
Adrenal insufficiency (congenital adrenal hyperplasia, w ambiguous genitalia in females)
DX vomiting - infants
Sepsis/infection Lesions of GIT/obstruction (malrotation, strangulated inguional hernia, pyloric stenosis) GORD Coeliac Gastroenteritis Intussception (3-12mo)
TX enuresis
Education and reassurance
Alarms worn at night Wetting diary Reward system/star chart Regular toileting Avoid caffeine Alarms Treat constipation/fecal incontinence and exclude UTI
Meds if resistant to conservative Mx:
Desmopressin (synthetic ADH/vasopressin analogue) - Child should NOT drink overnight (risk hyponatraemia)
Anticholinergics (oxybutynin)
Risk factors for DDH
o/e - SIGNS
INX
rf
○ Breech presentation
○ Positive family history of DDH
o/e
§ Ortolani - detects dislocated hip reducing during exam
§ Barlow - detects dislocating or subluxing during exam
§ Positive tests are ones in which ‘clunk’ is felt (click/popping)
§ Other signs to look for:
□ Discrepancy in leg length
□ Asymmetrical thigh skin folds (also present in 25% normal babies)
○ Ix: ultrasound <6months
+/- X-rays > 6 months
Commonest organisms for meningitis
<2 years old
§ Group B strep (pyogenes)
§ E coli and other GNB
§ Listeria monocytogenes
>2 years old § above § Strep pneumoniae § Neisseria meningitis § HIB (in unimmunised children)
What is a febrile convulsion?
- what is assoc with?
- prognosis
A type of fit due to rapid rate of temp rise above 39deg. Most are not serious.
Age-limited predisposition to seizures (mostly 5mo-2yrs)
Often with ear infections or URTi/UTI, viral exanthem.
Family history of seizures (30%) - same mutation in neuronal ion channel gene
Usually full recovery with no permanent damage/future epilepsy/mortality or morbidity. Incr risk of FURHTER febrile seizures.
Instructions for parent re: febrile seizure
Move away from danger. Nothing in mouth.
Place on side.
Note the time.
If never happened before call an ambulance or take to hospital for obs.
If > 5 mins or two in a row call an ambulance.
Give calpol/paracetamol.
Get treatment for cause of fever.
Make sure vaccinations are up to date.
Differentials for an irritable baby who is sleeping poorly
Colic
GORD/physiological reflux
Poor maternal/child relationship
Cow’s milk protein allergy
Features of colic
PURPLE CRYING Peaks at 6-8 weeks Unexpected Resists soothing Pain-like face Long-lasting (crying for >5 hours a day at times) Evening (sleep deficit is at peak)
Management of physiological reflux in infants
Reassirance (likely to resovle spontaneously)
Raise head of head
Avoid overfeeding - small freq feeds
Thicken formula
Omeprazole is just a bandaid - decreases acidity but doesn’t prevent reflux.
Features of asthma
SX
Signs
SX:
Wheeze and SOB
Responsive to salbutamol
Chest tightness, coughing (worse at night and in morning)
Signs:
- tracheal tug, WOB
- prolonged exp. phase
- exp wheeze
- tachypnoea
- decr RR and absent wheeze, decr breathe sounds in severe asthma
Most common causative agent of acute otitis media.
What would you see on ear exam?
How do you treat?
Strep pneumonia most common (H. influenza and moraxella catarrhalis)
See red bulging TM, presence of middle ear fluid
Analgesics. Limited value in treating w antibiotics as pain resolves in 2-7days
What are the bag bugs you have to watch out for that can cause pharyngitis?
Defining features
- EBV
- exudative tonsillitis assoc w cervical lymphadenopathy and generalised flu-like SX - HSV-1
Mucosal ulceration - Enteroviruses (Coxsackie A/B, echoviruses)
- assoc w oral ulcers and rash - Strep throat (pyogenies)
- exudative tonsilitis, strawberry tongue, widespread erythematous rash, tender enlarged cervical lymph nodes, high fever
What is ‘croup’?
Presentation
Aetiology
MX
Laryngotracheobronchitis
Presentation: barking cough +/- stridor on exertion (at rest = severe)
Aetiology: Parainfluenza
Mx: supportive treatment for most kids
- If stridor at rest, single dose of oral DEX then Observe for half an hour post steroid administration. Discharge once stridor-free at rest.
- If severe: O2, IM/IV dex, neb adrenaline, intubation or tracheostomy
If good improvement, observe for 4 hours post adrenaline. Consider discharge once stridor free at rest.
If deterioration/no improvement, give further adrenaline and consider admission or transfer as appropriate.
Features of autism
- Problems w socialisation
- poor eye contact
- difficulties w gestures
- not responding to name
- failure to socialise w others - Problems w communication
- limited use of language
- no imaginative play or social imitative play - Repetitive or obsessive behaviours
- repetitive play
- inflexible, repetitive use of language
- unusually obsessions w inflexible and limited interests
- self-stimulating behaviours (toe walking, hand flapping, jumping in place, making sounds, grinding teeth etc)
Asthma management plan (and what features define each stage?)
- mild
- moderate
- severe
- critical
1 dose salbutamol: 6 puffs if <6yo or 12 puffs if >6yo
- mild: 1 dose salbutamol and review after 20min. If good response, D/C on salbutamol PRN. Poor response, treat as moderate
- Moderate (incr WOB, disrupted sentences, tachycardia): Salbutamol 1 dose every 20min for 1 hour. review 10-20 min after 3rd dose to determine freq of next dose.
O2 if saO2<92% - Severe (agitated/distressed, marked WOB and limitation of speaking ability): Salbutamol 1 dose every 20min for 1 hour -> if responding, incr time between doses. If not responding, continue dosing even 20min.
+ o2 as above.
+/- atrovent via MDI/spacer every 20min for 1 hour only.
+/- IV Mg sulfate
+/- IV aminophylline - Critical (silent chest, confused/drwosy, no talking)
- O2
- Continuous nebuliser salbutamol
- Nebulised iprotropium (3x in 1st hour only)
- IV methylpred
- IV Aminophylline and MgSulfate
+/- ICU admission
+ 3 days oral pred with each (2mg/kg day 1 (in hosp) then 1mg/Kg day2,3)
Stridor
-differentials
- Inx?
Acute
- most common acute cause in kids is CROUP
- retropharyngeal abscess
- peritonsillar (quinsy) abscess
- laryngeal trauma
Persistent
- laryngomalacia most common cause of persistent stridor
- subglottic stenosis
- subglottic haemangioma
INX: only if stridor is persistent with an expiratory component (severe) = bronchoscopy
Differentials for wheeze
Since birth:
- airway malacia (tracheomalacia or bronchomalacia)
Gradual onset SX
- Asthma
- Recurrent viral-induced wheeze
- Cystic fibrosis
- Cardiac causes
Sudden onset SX
- LRTI (bronchiolitis, viral pneumonitis, bacterial bronchitis)
- Inhaled foreign body
Pre-pregnancy counselling - things to cover
- Identify risks to women’s fertility and pregnancy outcome
- age, BMI, smoking, STIS, substance abuse
- obstetric HX (ectopics, M/C)
- pap smears UTD
- medical HX - diabetes, asthma, epilepsy, thyroid, HTN, anaemia
- Medications (teratogens)
- fam hx thrombophilias, obstetric compl
- Immune status, vaccinations
- psychosocial (job, partner, home, MH, safety) - Education and Optimise health
- family planning (timing w ovulation - body temp and vag dc)
- supplements: folate, vit D, Ca, iron
- stop smoking, drinking, illicit drugs
- vaccines (MMR +/- varicella, influenza)
- weight loss
- Optimise chronic disease
- Aspirin if previous pre-eclampsia/TA/recurrent MC or IUGR
- Avoid teratogenic medications (Lithium in T3, warfarin, anti epileptics esp. sodium valproate and carbemazpine, ACEi)
- Diet (food hygiene, avoid pasteurised dairy, soft cheeses, uncooked meat, seafood)
Causes of anovulation or oligomenorrhoea
and management of each
Normal FSH (MX: lifestyle - weight loss, diet +/- ovulation induction)
- Obesity
- PCOS (+/- metformin)
Incr FSH (ovarian failure) - MX: IVF
- Age >45
- iatrogenic (radio/chemo)
- autoimmune (SLE, RA)
- Genetic (45XO, fragile X etc)
Decr FSH (HPO failure) - MX: lifestyle +/- ovulation induction
- anorexia, stress, chronic illness, over-exercising
- Pituitary tumour
- infiltrative disease (sarcoid)
Idiopathic (Mx: IVF)
Initial investigations for infertility
Hormones (FSH, Lh, oestrogen, androgens) Genetic karyotype +/- CF screen (males) Semen analysis (men) Imaging - USS testes; ovaries, uterus
Causes of female infertility
Egg factors - Advanced maternal age is #1!; aneuploidy
Anovulation (obesity, PCOS, stress, illness, anorexia, iatrogenic, autoimmune etc)
Endocrine - hypothyroid, hyperprolactinoma
Anatomy
- Mullein abnormalities
- Endometriosis
- Chronic infection (PID), scarring
- Fibroids (distortion)
Idiopathic/unknown
Causes of male infertility
Sperm - poor sperm count or abnormal sperm Genetics - CF or Kleinfelter Hypo-gonadism Vasectomy/testicular removal previously Varicocele, torsion, undescended testes Anabolic steroids
management - male infertility
Lifestyle - stop smoking, drinking, increase exercise and dietary antioxidants
Intra-cytoplasmic sperm injections (donor sperm)
Management of infertility
- Lifestyle - weight loss, exercise and diet (PCOS, obesity and incr sperm count)
- Ovulation induction (for PCOS, obesity, HPO failure)
- Clomiphene first line for PCOS; Letrozol; FSH; pulse dose LH/GnRH analogue/HCG triggers ovulation - IVF (for ovarian failure)
- Serum AMH predicts response to IVF - Cryopreservation (if <35years old)
- Consider male-infertility and Tx for that
What is HELLP syndrome?
definition + SX
A complication/variant of pre-eclampsia
Features: Haemolysis
Elevated liver enzymes
Low plt count
Sx - malaise, epigastric pain, RUQ tenderness (from liver dysfunction and capsular distention) \+Ft of PE: N and V Headache Swelling/oedema HTN, proteinuria
Criteria for diagnosis of PCOS
SX
Rotterdam criteria: 2 of the following
- Oligomenorrhoea reflecting an ovulation
- Hyperandrogenism (clinical or biochemical with incr free testosterone and decr SHBG)
- Polycystic ovaries on USS
Obesity Acne Hirsutism Sub fertility Oligo or anovulation
Criteria for diagnosis of PCOS
SX
Rotterdam criteria: 2 of the following
- Oligomenorrhoea reflecting an ovulation
- Hyperandrogenism (clinical or biochemical with incr free testosterone and decr SHBG)
- Polycystic ovaries on USS
Obesity Acne Hirsutism Sub fertility Oligo or anovulation
Management of PCOS
Diet and exercise firstling
Rest of MX depends on SX
- Oligomenorrhoea/anovulation (COCP to restore ovulation; cyclic progestins ex: IUD; metformin)
- Hirsutism (Diane trial for 6 mo 1st line; Spironolactone 2nd line; laser therapy, creams, doxycycline)
- Subfertility (diet and exercise, smoking cessation, folate supplement; ovulation induction ex: clomiphene +/- metformin)
- Cardiometabolic risk (metformin)
What additional antenatal care considerations do women pregnant w twins need?
Education/counselling around additional risks (fetal + maternal GDM, PE, APH, PPH, depression, anaemia, marital problems) and support services
Nutritional advice - incr requirements of energy, protein, folate, Ca, iron,
Aspirin from 12-36 weeks as PE prevention
Early GTT at 12 weeks if other RFs for GDM
MX of ectopic
If in shock: emergency laparotomy
Not in shock:
- If HCG<1000: Admit for Observation, await natural resolution (betaHCG and USS monitoring)
- If HCG>1000 or keeps rising:
Medical (for small tubal ectopics and minimal bleeding): Methotrexate IM
Surgical (for large ectopics or IU bleeding): laparoscopy and salpingectomy/salpingostomy
Follow up: serum B-HCG on days 4 and 7, should decr to ensure complete removal
Psych support
Causes of miscarriage
OLD AGE (mum and dad) -> chromosomal abnormalities (aneuploidy or 45XO)
Infx (TORCH)
Maternal disease - endocrine (GTM, DM), cardiac, renal, thrombophilia, HTN, autoimmune (SLE, coeliac), APLS
Anatomical - fibroids, ashermanns, cervical incompetence, bicorneate, subseptate
Lifestyle - smoking, alcohol, medications, drugs, obesity/anorexia
Trauma
What is adenomyosis
What are risk factors?
Endometrial glands found WITHIN myometrium (normal line the outside)
RF: middle aged (30s, 40s)
- multiparous women
Causes of abnormal menstrual bleeding
PPALM COEIN
Pregnancy - ectopic, miscarriage, normal Polyps Adenomyosis Leiomyosis /fibroids Malignancy Coag disorders (VWd, platelet disorders, factor 5/6/10 deficiency)
Ovulatory dysfunction (an ovulation, PCOS, CAH, thyroid disease, prolactinaemia, hypothal disorders)
Iatrogenic, infections
(anticoagulants, antiplatelets, OCP, HRT)
Endometrium (dysfunctional uterine bleeding- anovulatory or ovulatory) - MOST COMMON
Not classified (trauma, hepatic, infections, localised lesions)
- 2 Types of Dysfunctional uterine bleeding
- and underlying pathophys
- type of endometrium on histology in each case
Ovulatory
- ? due to excessive prostacyclin production -> incr vasodilation and decr platelet aggregation in the context of a SECRETORY endometrium
Anovulatory
- Lack of ovulation -> no CL -> no progesterone -> endometrium continues to thicken under influence of unopposed oestrogen until it outgrows blood supply, then undergoes necrosis and shedding -> cycles are long and irregular
- PROLIFERATIVE endometrium
DDX intermenstrual bleeding or post coital bleeding
Consider local cause
- polyps
- infection
- IUCD
- uterine or cervical cancer
- perimenopausal (anovulation)
Associated features to ask on history of abnormal bleeding (not including associated features)
Bleeding between periods or after intercourse?
Painful periods or pain with intercourse? Deep/superficial; always or recently
Faint/light headed/sweating/fatigue/palpitations -> anaemia
Pressure/frequency/distension -> fibroids/mass
Endocrine SX (weight changes, hair growth, acne) -> thyroid/PCOS
Easy bleeding/bruising -> bleeding disorder
Sexual partners, condom use, discharge, pelvic pain -> PID/endometritis/pregnancy
Last pap smear -> cervical cancer
Medications (incl contraception and blood thinners i.e. warfarin and aspirin)
Treatment for abnormal bleeding
Treat any underlying causes (e.g.: thyroid)
- Medical
- Anti PGE (NSAIDs, mefanamic acid/ponstan)
- Tranexamic acid (antifibrinolytic to reduce flow)
- Hormonal (COCP, depot provera, GnRH analogue)
- Mirena IUD - Surgical
- Endometrial ablation (+ tubal ligation)
- Hysterectomy (+/- oophorectomy)
What women are indicated for endometrial ablation
What women shouldn’t this be used on?
Sx of abnormal bleeding
- perimenopausal ideally (NOT in women who want to become pregnant)
- endometrium can grow back but isn’t as luscious as it was previously -> can lead to IUGR
What is the most common cause of teenager w menorrhagia?
What are other relatively common causes?
Anovulatory dysfunctional uterine bleeding (especially within first 18 months after menarche)
Bleeding disorder (10-20%) PCOS, thyroid disorder
Pregnancy
Local uterine/cervical causes rare
Causes of secondary dysmenorrhoea
Endometriosis Adenomyosis Intracavity mass (IUD, polyp, fibroid)
MX of endometriosis
Do nothing (SX aren’t severe, don’t impact QOL)
Pain relief/analgesia
Hormonal (OCP, progestins, GNRH analogues)
Surgery
- endometrial ablation or excision
- hysterectomy
Presentation of endometriosis
Cyclical pain: dysmenorrhoea, mid cycle pain, premenstrual pain
Pain on void/defecation w period
Provoked pain (pain w sex, tampon insertion, vaginal examination)
Infertility
Asymptomatic
Mx of adenomyosis
Tx is about QOL
Do nothing
Medication
- Analgesia (NSAIDs)
- Hormones (OCP, progestin, GNRH analogues)
- Mirena
Surgical
- hysterectomy
- myomectomy
- ? endometrial ablation
Classic presentation (SX and signs) of adenomyosis
SX
- menorrhagia
- dysmenorrhoea
Signs
- bulky uterus
- uterus tender on bimanual palpation
Treatment primary dysmenorrhoea
Do nothing
Analgesics - NSAIDs
Hormones (OCP, progestins, GnRH analgoes)
Mirena IUD
Hysterectomy once completed family (radical)
Acupuncture
Smooth muscle relaxants: nifedipine, GTN, buscapan (can cause postural hypotension! LOC etc)
3 common pathological causes of abnormal vaginal discharge
- trichomonas vaginalis = trichomoniasis (vaginal itching and irritation + profuse sometimes green frothy discharge)
- Candidiasis (severe vulvovaginal irritation assoc w thick cheese discharge)
- Bacterial vaginosis (no SX or thin greyish discharge w fishy smell)
What is PID? How does it present?
What main organisms cause this?
Infection of more than one pelvic organ
Presentation:
Severe bilateral lower abdo tenderness and pain
Guarding
Cervical excitation
Fever +/- rigors
Cl -> mucopurulent discharge, dysuria, inter menstrual bleeding
N.Gon-> dysuria, frequency, purulent discharge
- Cl. trachomatis
- Neisseria gonorrhoea
Causes of PPH
4 Ts
Tone: uterine atony, distended bladder.
Trauma: lacerations of the uterus, cervix, or vagina.
Tissue: retained placenta or clots.
Thrombin: pre-existing or acquired coagulopathy.
Investigations and management for suspected adenomyosis
USS and MRI (more sensitive)
Mx
- Hormonal treatment to induce amenorrhoea/reduce flow (IUCD etc, GnRH analogues)
- Hysterectomy
What is adenomyosis
What are risk factors?
Endometrial glands found WITHIN myometrium (normal line the outside)
RF: middle aged (30s, 40s)
- multiparous women
Mx leiyomyoma
Only treat if symptomatic! Mx depends on symptoms
- SX-atic treatment can manage heavy/irregular MB (COCP, NSAIDs, tranexamic acid)
- Hysteroscopic resection if sub mucous
- Myomectomy (remove single specific fibroid)
- Embolisation (blood blood supply to single problematic fibroid)
- Ablation (U/S beam under MRI guidance destroys fibroid tissue)
- Hysterectomy if resistant to treatment
Contraception options postpartum
when do you need this from?
4 weeks postpartum
progesterone only minimill
condoms
mirena
implant
COCP ok >day 25 if NOT breastfeeding (oestrogen CI in breastfeeding due to incr risk VTE)
Benefits of breast feeding
For mum - decr premenopausal breast cancer and ovarian cancer risk, contraception, osteoporosis, faster weight loss
for bub - decr RTIs, gastro illnesses, diabetes, obesity, HTN, CV disease, NEC, SIDs, incr IQ
Contents of breast milk
Proteins Ig Fats (TGL, fatty acids) Carbs (lactose, galactose, glucose) Minerals Electrolytes vitamins water
Complications of breast feeding
Cracked/grazed/bleeding nipples (incorrect attachment)
Engorgement (req expressing)
Low supply
Mastitis (keep feeding to drain breast + abx if unresolved in 12 hours)
Breast abscess (drain)
Definition and causes of 2dary PPH
Significant blood loss 24hours-6 weeks after birth
Causes
- Infx (endometritis, w GAS, GBS etc)
- Retained products
Sx/signs of endometritis
Postpartum bleeding abdominal pain Malodorous lochia fever tachycardia tender bulky uterus
Methods to terminate pregnancy
1st timester
- Surgical D&C - surgical and anaesthetic risks
- Medical: misoprostil (PGE analogue) or mifepristone (PR antagonist/GC and androgen antag) - painful and takes 3 days
2nd trimester
- DandC - surgical risks
- Medical: IOL + KCL + mifepristone + misoprostil - long traumatic process ~5d
Features of trisomy 21
low iQ short stature congenital abnormalities Dysmorphic features Heart and hearing problems 1/2 are FDIU
What causes late decelerations?
FEtal hypoxia and acidosis, usually due to
reduced uteroplacental blood flow: causes include…
Maternal hypotension
Pre-eclampsia
Uterine hyperstimulation
What does sinusoidal CTG pattern indicate?
Severe foetal hypoxia
Severe foetal anaemia
Foetal/maternal haemorrhage
What are variable decelerations caused by?
They are most often seen during labour and in patients’ with reduced amniotic fluid volume.
Variable decelerations are usually caused by umbilical cord compression¹:
What do shoulders of deceleration indicate?
“shoulders of deceleration“.
Their presence indicates the foetus is not yet hypoxic and is adapting to the reduced blood flow. Reassuring feature
What are accelerations?
Accelerations are an abrupt increase in baseline heart rate of >15 bpm for >15 seconds.
The presence of accelerations is reassuring.
What is normal variability?
what is reduced variability? absent?
6-25.
Reduced <=5
Absent <=3
Non reassuring if >45-60min duration
What causes reduced variability?
Reduced variability caused by:
- fetal seeing (last <60min)
- maternal sedatives (opiates / benzodiazepines / methyldopa / magnesium sulphate)
- Foetal acidosis (due to hypoxia) – more likely if late decelerations are also present
- Foetal tachycardia
- Prematurity – variability is reduced at earlier gestation (<28 weeks)
- Congenital heart abnormalities
Causes of prolonged (>2min) severe bradycardia are
Prolonged cord compression Cord prolapse Epidural and spinal anaesthesia Maternal seizures Rapid foetal descent
CTG framework
DR C BRAVADO
DR - define the risks Contractions Baseline Rate (110-160 normal) Accelerations (>15 bpm for >15sec) Variability (5-25 normal) Decelerations Overall impression
definition of Small for gestational age and causes
<10th centile
Causes:
- normal (tracking growth curve, small parents, previous small babies, normal USS findings, symmetrical)
- Incorrectly diagnosed/dates wrong
- Abnormally small (chromosomal/structural/genetic syndrome)
- IUGR (fail to reach growth potential, usually due to uteroplacental insufficiency)
Pathophysiology of GDM
How does this lead to fetal macrosomia?
Placental hormones cause a decrease in insulin sensitivity. At the extreme end you get maternal insulin resistance (tissues no longer responding to insulin so glucose isn’t taken into cells and levels in blood rise).
Maternal hyperglycaemia -> fetal hyperglucaemia -> fetal pancreas starts producing own insulin -> incr glucose uptake into fetal tissues -> incr fetal growth
RF for GDM
Age >35yo FHx PCOS Obesity Previous GDM pregnancy Certain ethnicities
Pathophys of Pre eclampsia
Disorder of the placenta
placenta demands more O2 and nutrients than mother can provide -> hypoxic placenta -> releases toxic products which damage mum’s vasculature, causing vasospasm and vasoconstriction -> HTN and ischaemia to organs
MX of pre-eclampsia
ADMIT
- Stabilise w BP control (if BP >= 160/100 -> labetalol, methyldopa, nifedipine)
- MgSo4 as anticonvulsant (monitor serum levels)
- monitor fluid balance, renal function
Fetal surveillance - severity dictates timing of delivery (maternal or fetal deterioration ->delivery)
Ensure mum is stable before delivery
- NVD if stable mum and bub
- LUSCS if unstable mum/bub, prima, premmie etc
How do you diagnose GDM?
Universal 28week 2nd trim screening for all women
- OGCT (non-fasting) - if BSL >7.8 -> 2.
- OGTT (fasting) - GDM if fasting >=5.5 and/or 2hr BSL >=8
Risks of ovulation induction
Multi pregnancy ovulation hyperstimulation (bloating, nausea, diarrhoea, thirst, decr urine output, abdo pain)
Newborn exam
General inspection
Skin (pallor, cyanosis, jaundice, rashes, bruises, skin marks)
Growth parameters
Palpate suture lines and fontanelles
Face - asymmetry/dysmorphia?
Ears, mouth (palate and rooting/sucking reflex), red reflex, pupils
Hands - # palmar creases, # fingers
Grasp reflex
Brachial pulse
Tone of upper and lower limbs
Chest - Ausculate heart and lungs
Abdomen - palpate, auscultate
Femoral pulses
Genitals (in boys, both testes present? position of meatus)
Hips - Barlow’s and Otoloni’s tests
Anus patency
Spine (alignment; hair pits and sacral tufts assoc w spina bifida)
Stepping reflex
Check head lag
Moro reflex
What might an absent red light reflex indicate?
Immediate ophthalmology referral as it may suggest congenital cataracts or rarely retinoblastoma
Causes of failure to thrive FTT (5)
-
MAY BE PSYCHOSOCIAL so take thorough social hX
- blunts GH response - Inadequate intake
- Neglect
- Low SES
- Poor diet - micronutrient deficiencies
- inability to suck/swallow - Inadequate digestion, absorption
- coeliac
- CMPA
- CF
- pancreatic, cholestatic issue
- Giardiasis
- Diabetes - Incr metabolism
- Carcinoma
- Hyperthyroid
- Chronic disease (resp, cardiac, renal, GI) - Prenatal issues
- prematurity
- maternal illness/drugs/smoking
- IUGR
- chromosomal abnormalities
Investigations for short stature/FTT
Bone scan
+/- karyotype if female (?45XO in female w short stature and delayed puberty)
Bloods: FBE, UEC, LFTs, ESR
- TFT, coeliac serology
- Nutrition: CMP, Fe, vit D, B12, folate, IGF1
Urine analysis (infx, renal disease)
MX for short stature
- education/reassurance
- change diet
- treat any underlying pathology
- +/- GH therapy
- psychosocial support
Causes of short stature (3) and how is bone age related to chronological age in each?
is the growth velocity normal or abnormal in each?
- Familial Short Stature (bone age = chronological age)
Normal growth vel.
Normal puberty onset - Congenital Delayed Growth (bone age < chronological age)
Normal growth vel.
Delayed puberty
normal adult height when reached - Pathological (endocrine PICNICS)
Abnormal growth vel.
Pathological causes of delayed growth
Endocrine PICNICS
Endocrine - hypothyroid, GH deficiency or insensitivity, Cushing’s disease, adrenal insufficiency
Psychosocial
Iatrogenic - exogenous steroids, spinal
Chronic disease - GI (coeliac, IBD); renal (CKD, RTA), cardiac (CHD), JIA, tumour
Nutritional disease
Intrauterine growth restriction
Chromosomal - Turner syndrome, Down syndrome, Prader Willi
Skeletal abnormalities (achondroplasia)
What is the most common haemolytic cause of newborn jaundice?
What is the most severe cause?
ABO incompatibility
Mother is usually type O with baby type A
Rh disease is more severe
Newborn baby is jaundiced and has pale poos. what do you suspect and how do you investigate this?
why is it important to treat early?
Biliary atresia
US of liver/biliary tree to investigate for obstructive causes
Investigate within 6 weeks otherwise results in irreversible liver damage
When is newborn jaundice always pathological
If it occurs within first 24 hours after birth (suspect haemolysis or sepsis)
Conjugated hyperbilirubinaemia
Mx of newborn jaundice
- Observe/watch
- Blue light phototherapy (converts bilirubin into water-soluble form that can be excreted in bile and urine)
- Exchange transfusion (replace baby’s blood w donor blood to decr bilirubin levels rapidly)
SBR Levels at which these are performed are determined using standard hospital monogram
Abi if sepsis suspected
Causes of pathological vs benign jaundice
Benign
- Physiological (resolves around 1 week post birth, peaking at 3 days)
- Breast milk (peak at 2 weeks)
Pathological
1. Haemolytic
- Incr Haem load (haemorrhage, polycythaemia, swallowed blood)
- Impaired hepatic uptake and conjugation (Gilbert, hypothyroid, drugs etc)
- Mixed (prematurity, sepsis, infants of diabetic mothers, asphyxia)
- Structural - biliary atresia
Complication of jaundice
kernicterus (neuronal death caused by toxic unconjugated bilirubin crossing the BBB) -> manifests as bilirubin encephalopathy
Can lead to death or survival with cerebral palsy (neurodevelopment impairment)
Haemolytic causes of jaundice
Immune
- ABO and Rh blood group incompatibility
- Drug-induced
Acquired
- bacterial sepsis
- congenital intrauterine info
Hereditary
- G6PD deficiency
- Hereditary spherocytosis
Features ADHD
Inattentive
Hyperactive
Impulsive
Poor planning
Features of ODD
Loses temper
Resistant to authority
Deliberately annoys
DC criteria for asthma
Parent and child education
Technique review/education for MDI+spacer
Scripts if needed
Written asthma action plan
Assess patient - no WOB - haem stable - adequate oral intake Salbutamol therapy stretched to >=4 hourly
Organised OP or GP R/V
Chronic cough ddx and first line inx
Asthma
(Post-)Viral or bacterial URTI or LRTI
Cardiac (pulm HTN, pulm oedema)
Bronchiectasis (CF, primary ciliary dyskinesia, immunodeficiency, foreign body etc)
Aspiration
Chronic/less common infx (Tb, pertussis, mycoplasma, atypical pneumonia)
Interstitial lung disease (rheumatic diseases, cytotoxic, drugs, radiation)
GOR
Psychogenic
FIRST line Ix: CXR and spirometry if >6yo
Investigations of newborn jaundice
FBE + blood firm and reticulocytes
SBR
Indirect and direct Coombs test
RF for asthma
atopy
Family hx asthma
RSV bronchiolotiis as a child
Exposure to cigarette smoke, allergens, pollution
Classifications of asthma and corresponding therapy
Intermittent - PRN ventolin
Persistent: PRN ventolin +
- Mild: low dose CS inhaler
- Moderate: med dose CS inhaler +/- LABA or montelukast
- Severe: high dose CS inhaler +/- LABA or montelukast +/- oral systemic CS
Causes of B12 deficiency in kids
+MX
Dietary deficiency (vegans) - in exclusively goat’s milk fed bubs
Malabsorption (coeliac, IBD, resection of terminal ileum)
Inborn errors of metabolism
Pernicious anaemia (inability to secrete intrinsic factor which is req for B12 absorption in terminal ileum)
MX - monthly B12 injections +/- iron and folate supplements if goat’s milk fed
Causes of anaemia
Microcytic
- iron deficiency
- chronic blood loss
- alpha thalassemia
- chronic disease
Normocytic
- acute large vol haemmhorage
- chronic disease
Macrocytic
- B12 or folate deficiency
- Hypothyroidism
- T21
- Leukaemia
- Myelodysplasia
Definition and DDX delayed puberty (boys and girls)
Both - hypopituitarism, chronic disease, malnutrition
Boys - no 2ndary sex characteristics by age 14
- Kleinfelter’s syndrome (XXY)
Girls - no 2ndary sex characteristics by age 13
Turner’s syndrome (45XO)
DDX fevers, rash and refusal to weight bear
JIA EBV Osteomyelitis Septic arthritis Leukaemia Lymphoma SLE Osteosarcoma
Examples of ACYANOTIC heart defects
1. L->R shunt VSD PDA ASD AVSD
2. Obstructive heart defects Pulmonary stenosis Aortic stenosis Coarctation of aorta Hypoplastic L heart syndrome
what are the 2 most common types of CHD in kids?
- VSD
2. PDA
What are SX of heart failure in a newborn?
tachypnoea
SOB and sweating when feeding
Failure to thrive
Incr WOB
What causes the ductus arterioles to close? when does this occur?
Why might it not close?
Closes in first 1-7 days post birth due to decreased circulating PGE2 and increased paO2, as well as muscle contraction
May fail to close in this period due to
- prematurity
- congenital malformation
What is the treatment for a PDA in a premature infant?
Indomethacin or other NSAIDs (inhibit PGE2 to promote ductal constriction and closure)
How do PDAs present?
Small PDAs generally asymptomatic. May have continuous murmur at upper L sternal edge.
Large PDAs present with L heart dilatation (displaced apex beat, parasternal heave) and progressive SX of heart failure.
+ Bounding pulses
+ Apical mid-diastolic murmur
Presentation of a VSD
Depends on the size
1. Small: pan systolic murmur @ L sternal edge rad to axilla BUT ASYMPTOMATIC at birth bc pressures between L and R heart are equal
- Large: left heart dilatation leads to displaced apex, parasternal heave
- SX of HF occur after lungs open up and L sided pressures > R.
(poor feeding, FTT, tachypnoea, incr WOB, hepatomegaly)
Note: L heart dilatation occurs because L heart has to work harder to generate the same CO w shunt present.
What investigations do you do if you hear a murmur in a baby?
CXR
ECG
ECHO is diagnostic
How do ASDs present?
Small ASDs go undetected (low pressure gradient across atria)
Large ASDs rarely symptomatic in childhood
-may cause Atrial arrhythmias in adulthood, and reduced exercise capacity
Because L->R shunt causes R heart enlargement ->
- parasternal heave
- ES murmur in pulmonary region with fixed splitting of A2 and P2
What is the treatment for ASD and when is it indicated?
Indicated if patient has RH enlargement
Transcatheter or surgical closure
How does AVSD present?
Tx?
Partial AVSD - behaves physiologically and symptomatically like ASD
Complete AVSD - presents like severe VSD (FTT, feeding difficulties, tachypnoea, WOB)
almost always needs surgical closure
When does cardiac failure onset in newborns with coarctation of aorta?
How might this present on exam?
When ductus arteriosus closes because then there is NO blood flow to the rest of the body.
Diminished/absent femoral pulses
unequal BPs between L and R arm
Examples of cyanotic heart defects
The 4 Ts:
- Tetralogy of Fallot
- Transposition of great arteries
- Tricuspid atresia
- Truncus arteriosus
What is the tetralogy of fallot and what 4 things comprise it?
Obstruction to RV outlfow tract + septal defect below obstruction such that blood can flow from RV to LV (R->L shunting)
§ 4 anatomical defects: □ Overriding aorta □ RV hypertrophy □ Pulmonary stenosis □ VSD
Clinical picture of tetralogy of fallot
Kids:
Gradual, delayed development of cyanosis
Delayed exercise tolerance, finger clubbing, growth retardation
Development of compensatory polycythaemia
Babies:
‘tet’ spells: cyanosis more obvious when baby is upset, crying
(Baby may go floppy, lose consciousness)
