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MD3 > Women's and CAH OSCEs > Flashcards

Women's and CAH OSCEs Flashcards

1
Q

SX pregnancy

A

Nausea
Tender breasts
Missed period
Urinary frequency

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2
Q

Naegle’s rule

A

Date of conception is first day of last normal period + 9 months and 7 days

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3
Q

Antenatal visit frequency

A

> 28/40: monthly
28-36: biweekly
36: weekly

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4
Q

Supplements pregnant women should take

A

Folate
Vitamin D
Iron
Ca

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5
Q

Routine bloods at first antenatal visit (12 weeks)

A 
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)

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6
Q

Components of combined down syndrome serum screen

A

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.

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7
Q

IF a women’s combined serum screen comes back as high risk, what is the next step in investigations for diagnosis?

A

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

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8
Q

when do routine USS in low-risk pregnancies typically occur.

A

Ultrasound @ 12 weeks: gestational age and down syndrome screen

18-20weeks: morphology and wellbeing

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9
Q

What bloods get done in the second trimester and when?

A

28 week bloods:

  • FBE
  • Oral glucose challenge
  • AB screen in Rh neg women (will need anti-D injections if no Anti-D detected)
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10
Q

Who needs anti-D injections and when are these given?

A

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

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11
Q

What 2 medical conditions do we screen for every visit and how do we do this?

A

Placental insufficiency - ask about fetal movements + SFH

Pre-Eclampsia - HTN (BP), proteinuria (urine dipstick) , oedema (exam/Hx)

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12
Q

What routine Inx get done in the third trimester and when?

A

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)
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13
Q

Advise to women in third trimester as to when to come to hospital

A

Contractions are regular and painful, occurring ~1x5min (2:10) OR:

  • DFM
  • Bleeding
  • SROM
  • Psychological distress
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14
Q

When does the GBS swab get done?

A

36 weeks, lower vaginal and anal swab

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15
Q

When does the oral glucose challenge test get done?

A

28 weeks

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16
Q

How do you assess fetal wellbeing antenatally (5)

A
  1. fetal movements
  2. maternal SFH
  3. USS
  4. Infection screen +/- karyotype (aneuploidy screen)
  5. CTG
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17
Q

Assessing fetal wellbeing in labour

A
  1. CTG
  2. fetal movement
  3. Doppler
  4. Fetal scalp blood sampling
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18
Q

what growth scan patterns do you see in IUGR babies?

GDM babies?

A

asymmetrically small: HC is relatively larger than AC

Asymmetrically large: AC to HC ratio high (due to glycogen deposits in liver)

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19
Q

Indications for elective C/S delivery for large babies

A

If EFW >97th centile
GDM
High AC: HC ratio (risk of shoulder dystocia)

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20
Q

Management of IUGR

A

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

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21
Q

Risk factors for ovarian cancer

Protective factors

A
  • 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

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22
Q

Clinical présentation of ovarian cancer

A 
Bloating, abdo swelling
Abdo pain
Dyspepsia 
Urinary freq
Weight change
Irreg bleeding
SX metastatic disease: ascites, pleural effusions, SBO/LBO
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23
Q

Inx for suspected ovarian cancer

A

TVUSS

Bloods: CA125 and CEA ; hcG, LDH, alpha fetoprotein

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24
Q

Risk factors uterine cancer

A
  • Age
  • Caucasian
  • nulliparity
  • early menarche, late menopause
  • Hx infertility
  • HRT/tamoxifen
  • Obesity
  • Diabetes
  • PCOS
  • Endometrial hyperplasia
  • HNPCC
  • Endometrial polyps
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25
Q

Presentation of cervical cancer

A

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
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26
Q

Risk factors for cervical cancer

A 
SMOKING
Long term OCP use
HIV, immune suppression 
High parity
Chlamydia trachoma's, HSV infection
Uncircumcised male partner
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27
Q

What can HPV virus cause?

A 
Genital warts (warts elsewhere too, like plantar warts etc)
Cervical cancer 
Vulval/vaginal cancer
Anal cancer
Penile cancer
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28
Q

Natural history of HPV infection of cervix

A

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)

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29
Q

When is the guardasil vaccine given and what HPV strains does it protect against?

A

Given at 0, 2, 6 months of age

HPV 16,18,11

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30
Q

Management of LGSIL found on pap test

A

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

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31
Q

Management of HGSIL found on pap

A

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)

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32
Q

How might an ovarian germ cell tumour present?

A

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)
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33
Q

How does GTD present?

A

Usually presents as miscarriage <10weeks and is diagnosed on post-mortem histopath

Sx of pregnancy

Early pregnancy PV bleeding

irregular vaginal bleeding

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34
Q

What hormone does GTD produce and how is this helpful clinically?

A

produces hCG, used as a tumour marker for diagnosis (serial hCG) and follow-up/monitoring

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35
Q

Which type of benign molar pregnancy has a higher risk of progression to neoplasia?

A

Complete

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36
Q

When does GBS sepsis present and what are risk factors for the congenital infection?

A

First 24 hours of life

RF: premature, PROM >18 hours, maternal fever, GBS positive mother (carries it in her GI/GU tract)

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37
Q

MX of a GBS positive mother

A

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

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38
Q

Consequences of maternal parvovirus B19 infection in pregnancy

A

If primary infection in pregnancy, small risk (3-5% of maternal infections) of fetal hydrous and intrauterine death secondary to fetal anaemia

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39
Q

Risk factors for chorioamniotis

A

PROM
Prolonged labour
Multiple intrapartum VEs
Internal fetal HR monitoring (scalp electrode)
Genital tract infections (STIs, GBS positive)

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40
Q

Clinical features of chorioamnionitis

A 
Maternal fever or fetal tachycardia
Uterine pain/tenderness
PV blood loss
Preterm labour
Malodorous or purulent amniotic fluid 
FBE: Incr WCC + incr CRP
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41
Q

Management of chorioamnionitis

A

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)

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42
Q

Pathophys of menopause

how do hormones change with this?

A

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

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43
Q

Symptoms of menopause and what do they relate to?

A

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

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44
Q

Management of osteoporosis in menopause

A

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)

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45
Q

Risk factors for osteoporosis

A 
Low BMI (decr fat - decr oestrogen which is protective)
Smoking
Family Hx
excessive caffeine
steroids
IBD/malabsorption
Decr VitD
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46
Q

Definition of menopause

normal age range

A

final menstrual period, determined after 12 months of amenorrhoea
normal age range: 45-57

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47
Q

Non-hormonal management of menopause

A

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

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48
Q

Hormonal management of menopause

A
  1. 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

  1. 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)
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49
Q

SE of HRT and CI

A

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
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50
Q

Investigations for premature menopause (<45)

A

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

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51
Q

Differentials deep dyspaerunia

A 
Endometriosis
Adenomyosis
Adhesions
PID
Fibroid 
Neoplasia
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52
Q

Differentials superficial dyspareunia

A

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

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53
Q

Aetiology post-menopausal bleeding

A

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

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54
Q

Inx and Mx of post-menopausal bleeding

A

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
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55
Q

Vaccines given at birth

A

HBV

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56
Q

Vaccines given at 2,4,6mo

A

DTPa (Diptheria, tetanus, whooping cough)

HIB

IPV (inactive polio vaccine)

HBV

PCV (13v pneumococcal conjucate)

RV (Rotavirus)

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57
Q

Vaccines given at 12mo

A

MMR (measles, mumps, rubella)
HIB
MenCCV

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58
Q

Vaccines given at 18mo

A

VZV (chickenpox)
MMR (measles mumps rubella)
DTP

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59
Q

Vaccines given at 4y

A

DTPa (diphtheria, tetanus, pertussis)

Polio

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60
Q

Vaccines given at 10-15y

A

DTPa (diphtheria, tetanus, pertussis)
VZV (chickenpox #2)
HPV

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61
Q

Side effects of vaccines

A
  • 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

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62
Q

Contraindications to vaccines

A

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
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63
Q

Gross motor milestones

A

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

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64
Q

Red flags for gross motor milestone

A

Not walking by 18mo

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65
Q

Fine motor milestones

A

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

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66
Q

Social and daily living skills milestone red flags

A

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

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67
Q

Language milestones

A 
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
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68
Q

Social milestones

A

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

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69
Q

DDX vomiting in 6mo year old

A

Overfeeding
GORD

Malrotation
Pyloric stenosis

Intussusception

Sepsis (lungs, UTI, GE)

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70
Q

features of malrotation

A

Early signs

  • Bilious vomiting (flour green)
  • Poor feeding

Late signs include: PR bleeding, abdominal distention and tenderness

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71
Q

What causes malrotation?

A

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

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72
Q

How do you diagnose malrotation?

What is the treatment?

A

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

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73
Q

When does malrotaiton w volvulus generally present?

A

50-75% within 1st month of life

90% within a year of life

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74
Q

Typical presentation of hypertrophic pyloric stenosis

A

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

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75
Q

When does pyloric stenosis typically present?

A

Peak 3-6 weeks old

But can occur 10 days-11 weeks

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76
Q

What metabolic derangements do you see in pyloric stenosis and why?

A

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)

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77
Q

What is intussception and what generally causes it?

A

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

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78
Q

Classic presentation of intussception

A

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.

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79
Q

Complications of intussception if not treated early

A

BO

Ishcaemia, Perf, shock

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80
Q

How do you diagnose intussception?

A

Clinical suspicion -> US (‘target sign’) is first choice

or AXR (?soft tissue mass ?absence of gas in caecal region)

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81
Q

Tx intussusception

A

<48 hour history in otherwise stable child = air enema reduction

> 48 history or peritonitic/septic child = laparotomy

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82
Q

Treatment pyloric stenosis

A

Fluid rehydration therapy and electrolyte replacement

  • 0.45% saline with 5% dextrose
  • Add K when baby is urinating

Non-urgent surgical referral

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83
Q

DDX for acute scrotum (red, painful, tender scrotum)

Immediate management

A
  • testicular torsion
  • torsion of appendix testies
  • epididymo orchitis
  • idiopathic scrotal oedema

Urgent surgical referral ?surgical exploration

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84
Q

Classic presentation of appendicitis

A

Colicky periumbilical pain migrating to RLQ and becoming constant

Assoc w :

  • anorexia
  • fever
  • nausea
  • d&v
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85
Q

Classifying seizures

A

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)

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86
Q

2 year old with incomplete immunisations at creche with fever and cough, coryza, conjunctivitis progressing to descending, blotchy raised (papular) rash
- diagnosis

A

Measles

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87
Q

Things that incr change of fit in epilepsy

A

Stress
Fatigue/lack of sleep
Alcohol
COMPLIANCE

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88
Q

DDX for generalised tonic clonic seizure (and what you would expect for each on history)

A

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

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89
Q

Upper limit of normal for axillary temp

A

Axillary > 37.2C

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90
Q

What do you do if a child comes in with a fever?

A 
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

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91
Q

What comprises a septic screen?

A

FBE, blood film
Blood and urine cultures
LP +/- CXR (if resp SX/signs)

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92
Q

What questions to ask on HX when a child comes in with fever

A 
Localising symptoms: 
cough
coryza
headache
photophobia
diarrhoea, vomiting
abdominal pain
joint symptoms

Travel history
Sick contacts
Immunisation hx

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93
Q

Presentation of meningococcus

A

Rapid onset
Fever
Flu-like SX (malaise, lethargy, vomiting, headache, myalgia, arthralgia)
Confusion

Rash (petechial/purpura)
Photophobia
Neck pain/stiffness

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94
Q

Differentials for child presenting with fever and petechial rash (previously well, onset this am)

A

Meningococcus if unwell/shocked/toxic

Viral infection (enterovirus, influenza)
HSP
ITP

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95
Q

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?

A

HHV6 (roseola)

No treatment required - self limiting.

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96
Q

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?

A

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

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97
Q

What are the clinical features of measles?

A

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

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98
Q

Management for measles

A

Supportive - fluids, panadol

MMR vaccine (2 doses) within 72 hours of exposure if >9mo

IVIG if <9mo or >9mo but >72 hours post exposure

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99
Q

Differentials for diffuse erythematous rash (sunburn-like) in child

A

Bacterial:
Toxic shock syndrome (Staph or strep)
Scarlet fever/Invasive GAS

Viral

Other:
Kawasaki disease
Antibiotics

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100
Q

What causes Scarlet fever?

A

Exotoxins from Group A Strep (pyogenies)

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101
Q

Clinical presentation of scarlet fever

A 
Exudative tonsillitis +/- pharyngitis
Confluent erythematous sunburn-like rash
Strawberry tongue
Circumoral pallor
lymphadenopathy
fever
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102
Q

Treatment of scarlet fever

A

Penicillin (oral) - to treat GAS

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103
Q

Features of Kawasaki disease

A

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)

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104
Q

Treatment of kawasaki disease

A

IVIG and low-dose aspirin

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105
Q

Complication of kawasaki disease

A

Coronary artery aneurysm

Higher risk of IHD

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106
Q

Features of infectious mononucleosis (glandular)

A 
FEVER
Exudative pharyngitis
Tonsillitis 
Lymphadenopathy
Splenomegaly
Palatal petechiae
Rash
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107
Q

Tx mono

A

None

Steroids only if airway obstructed due to tonsillar enlargement

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108
Q

Signs of resp distress in a newborn

A

○ 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

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109
Q

What is TTN?

RF?

A

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

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110
Q

Mx TTN

A

most babies settle in 24-48 hours with minimal handling and cot O2.
CPAP if acidotic, low sats, working hard to breathe.

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111
Q

What is infant RDS? Another name for it?

Who gets it (1 RF)?

Treatment?

A

= 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).

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112
Q

Characteristic CXR appearance of RDS/HMD

A

Hypo aeration, diffuse GROUND GLASS appearance, air bronchograms

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113
Q

RF mec aspiration

A

Post-term (>40 weeks)

Births involving fetal distress

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114
Q

RF for neonate sepsis

A

Maternal GBS positive
Maternal fever
Prolonged rupture of membrane (>=18 hours)

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115
Q

Abx coverage for neonatal sepsis (what bugs are you worried about?)

A

Gentamicin (listeria, e coli, HIB)

Benzyl-penicillin (GBS)

116
Q

Differentials for resp distress

A 
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 ?
117
Q

complications of genital prolapse

A

Hydronephrosis (obstruction of ureters in severe cases)

Urinary retention (outflow obstruction)

Faecal incontinence
Rectal prolapse
Haemmharoids

118
Q

SX of genital prolapse to ask about

A 
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
119
Q

Management of genital prolapse

A

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

120
Q

How do you assess the progress of a woman in labour?

A
  1. Abdo palpation hourly
  2. Contractions - duration, freq, intensity
  3. VE - 4 hourly (as long as membranes are NOT ruptured)
121
Q

Options for intrapartum pain relief

A

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)

122
Q

What defines Hyperemesis gravidarum. What complications do you have to watch for?

A

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)

123
Q

RF for hyperemesis gravidarum

A 
Previous HG
Multi-pregnancy
Molar pregnancy
Female embryos
Increase free beta HCG (molar pregnancies)
124
Q

Investigations for vomiting in pregnancy and why (ddx to consider)

A

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

125
Q

What is pre-eclampsia?

A

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)

126
Q

RF for Pre eclampsia

A 
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

127
Q

Clinical features of Pre Eclampsia

A

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

128
Q

Investigations for Pre Eclampsia

A

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)

129
Q

Definition of Eclampsia

A

Seizures assoc w PE due to hypo perfusion of brain

130
Q

Prevention of Pre Eclampsia.

Which women should get this?

A

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,

131
Q

Treatment of VTE in pregnancy

A

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

132
Q

Clin presentation GDM

A

Asymptomatic, picked up on routine 28 week GTT

SX of hyperglycaemia (polyuria, polydipsia)

Incr SFH

133
Q

MX of GDM

A

Multidisciplinary care
1. Education. Diabetic education nurse, dietician, endocrinologist, obs/gynae input

  1. Frequent self monitoring of capillary BSL (fasting <5mmol, 1hr post prandial <8mmol)
  2. Diet and exercise daily
    - Add insulin and/or sulfonyelurea/metformin if targets not met
  3. Antenatal Fetal monitoring
    - Additional routine growth scans
    - Regular clinical assessments of growth (SFH)
  4. Consider IOL/electice LUSCUS after 38 weeks if poorly controlled /evidence of fetal involvement
  5. Close fetal monitoring intrapartum
  6. Postpartum neonatal follow-up monitoring for jaundice, RDS, hypoglycaemia, hypocalcaemia
  7. Screening GCT early in future pregnancies
134
Q

Consequences of GDM

A

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)
135
Q

What is the definition of a miscarriage?
When is the risk of this highest?

SX?

A

Spontaneous loss of pregnancy <20weeks gestation

Highest risk <12/40

SX: lower abdo pain + PV bleeding

136
Q

Definition of recurrent miscarriage.

What investigations would you perform?

A

> 3 consecutive miscarriages

137
Q

Advice after a M/C

A

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)

138
Q

Risk factors for ectopics

A 
STIs
Smoking
Prior ectopic
Incr age
Prior tubal surgery/ligation
IVF
Progestogens
Contraceptive failures (pregnant with IUD)
139
Q

Presentation of ectopic pregnancy

A

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

140
Q

Inx for suspected ectopic

A

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

141
Q

MX of ectopic

A

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

142
Q

Impact of ectopic on future pregnancies

A

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

143
Q

CI to the COCP

A 
Women with IHD
Previous stroke, VTE
Breast cancer
Severe liver/biliary disease
Breast feeding with infants <6mo
Migraine with aura
144
Q

What happens if you miss one COCP pill?

What happens if you miss 2 or more?

A

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.

145
Q

Mechanism of action of the COCP

A

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
146
Q

Advice for starting the COCP

A

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)

147
Q

Risks vs benefits of the COCP

A

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
148
Q

Which women is the progesterone only mini pill good for?

A

Breast feeding women (COCP CI for babies <6mo)

Women in whom oestrogen is CI (breast cancer, risk of VTE etc)

149
Q

How does the mini pill work?

SE

A

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.

150
Q

How does the nuva ring work?

A

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.

151
Q

How does Depot Provera work?

Adv and disadv?

A

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

152
Q

What is implanon and it’s advantages and disadvantages

A

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

153
Q

How does the copper IUD work and what are side effects

A

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

154
Q

How does the progesterone IUD work and what are advantages and disadvantages?

A

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)

155
Q

Advice on natural family planning

A

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
156
Q

GI physiological changes in pregnancy

A

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)

157
Q

DDX genital itch (females)

A

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)

158
Q

What is bacterial vaginosis?

SX
Diagnosis
Tx

A

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.

159
Q

How does trichmononas vaginalis present?
What sort of bug is it?
How do you diagnose it?
How do you treat it?

A

Males - asymptomatic
Females - malodorous vaginal (frothy yellow-green fishy) discharge + ITCH

Protozoan parasite

Dx: high vaginal swab for microscopy and culture

Tx: oral metronidazole

160
Q

Chlamydia Trachomatis:

SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?

A

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

161
Q

Gonorrhoea

SX
What sort of bug is it?
How do you diagnose it?
How do you treat it?

A

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

162
Q

What HPV strains cause genital warts?

A

6 and 11

163
Q

Candida albicans

SX
DX
TX

A

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

164
Q

HSV

SX
How do you diagnose it?
How do you treat it?

A

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

165
Q

DDX constipation in kids

A

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)
166
Q

Causes of delayed passage of meconium

A 
Cystic fibrosis
Malrotation +/- volvululus 
Fistula
Imperforate anus
Down Syndrome 
Hirschsprung's
167
Q

Functional causes of constipation in kids

A
  • withholding behaviour
  • pain
  • anxiety
  • diet
  • dehydration
  • change in lifestyle (weaning onto solids, toilet training, starting school)
168
Q

Mx constipation in kids

A
  1. Change behaviour (toilet sits, position on toilet, stool diary)
  2. Diet - incr fluid and fibre, healthy diet
  3. Education
  4. Disimpaction if there is significant impaction that they are unlikely to pass (movicol adult doses as OP or colonlytely as IP)
  5. Laxatives

Regular review and monitoring

169
Q

Laxative medications used in children

A

Paraffin oil (softener)
and/or
Movivol or osmolax (osmotic laxatives)

170
Q

Laxative medications used in infants and neonates

A

Coloxyl drops (stool softener)

171
Q

DDX vomiting - older kids

A 
Migraine headache
Intracranial neoplasm (morning vomiting and headaches)
Acute appendicitis and peritonitis (>5yo)
Poisoning
Psychological (anxiety, stress)
Sepsis 
Meningitis/encephalitis
Pregnancy
172
Q

DDX vomiting neonates

A

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)

173
Q

DX vomiting - infants

A 
Sepsis/infection
Lesions of GIT/obstruction (malrotation, strangulated inguional hernia, pyloric stenosis)
GORD
Coeliac
Gastroenteritis
Intussception (3-12mo)
174
Q

TX enuresis

A

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)

175
Q

Risk factors for DDH

o/e - SIGNS

INX

A

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

176
Q

Commonest organisms for meningitis

A

<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)
177
Q

What is a febrile convulsion?

  • what is assoc with?
  • prognosis
A

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.

178
Q

Instructions for parent re: febrile seizure

A

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.

179
Q

Differentials for an irritable baby who is sleeping poorly

A

Colic
GORD/physiological reflux
Poor maternal/child relationship
Cow’s milk protein allergy

180
Q

Features of colic

A 
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)
181
Q

Management of physiological reflux in infants

A

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.

182
Q

Features of asthma

SX

Signs

A

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
183
Q

Most common causative agent of acute otitis media.

What would you see on ear exam?

How do you treat?

A

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

184
Q

What are the bag bugs you have to watch out for that can cause pharyngitis?

Defining features

A
  1. EBV
    - exudative tonsillitis assoc w cervical lymphadenopathy and generalised flu-like SX
  2. HSV-1
    Mucosal ulceration
  3. Enteroviruses (Coxsackie A/B, echoviruses)
    - assoc w oral ulcers and rash
  4. Strep throat (pyogenies)
    - exudative tonsilitis, strawberry tongue, widespread erythematous rash, tender enlarged cervical lymph nodes, high fever
185
Q

What is ‘croup’?

Presentation

Aetiology

MX

A

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.

186
Q

Features of autism

A
  1. Problems w socialisation
    - poor eye contact
    - difficulties w gestures
    - not responding to name
    - failure to socialise w others
  2. Problems w communication
    - limited use of language
    - no imaginative play or social imitative play
  3. 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)
187
Q

Asthma management plan (and what features define each stage?)

  1. mild
  2. moderate
  3. severe
  4. critical
A

1 dose salbutamol: 6 puffs if <6yo or 12 puffs if >6yo

  1. mild: 1 dose salbutamol and review after 20min. If good response, D/C on salbutamol PRN. Poor response, treat as moderate
  2. 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%
  3. 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
  4. 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)

188
Q

Stridor
-differentials

  • Inx?
A

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

189
Q

Differentials for wheeze

A

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
190
Q

Pre-pregnancy counselling - things to cover

A
  1. 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)
  2. 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)
191
Q

Causes of anovulation or oligomenorrhoea

and management of each

A

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)

192
Q

Initial investigations for infertility

A 
Hormones (FSH, Lh, oestrogen, androgens)
Genetic karyotype +/- CF screen (males)
Semen analysis (men)
Imaging - USS testes; ovaries, uterus
193
Q

Causes of female infertility

A

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

194
Q

Causes of male infertility

A 
Sperm - poor sperm count or abnormal sperm
Genetics - CF or Kleinfelter
Hypo-gonadism
Vasectomy/testicular removal previously
Varicocele, torsion, undescended testes
Anabolic steroids
195
Q

management - male infertility

A

Lifestyle - stop smoking, drinking, increase exercise and dietary antioxidants

Intra-cytoplasmic sperm injections (donor sperm)

196
Q

Management of infertility

A
  1. Lifestyle - weight loss, exercise and diet (PCOS, obesity and incr sperm count)
  2. Ovulation induction (for PCOS, obesity, HPO failure)
    - Clomiphene first line for PCOS; Letrozol; FSH; pulse dose LH/GnRH analogue/HCG triggers ovulation
  3. IVF (for ovarian failure)
    - Serum AMH predicts response to IVF
  4. Cryopreservation (if <35years old)
  5. Consider male-infertility and Tx for that
197
Q

What is HELLP syndrome?

definition + SX

A

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
198
Q

Criteria for diagnosis of PCOS

SX

A

Rotterdam criteria: 2 of the following

  1. Oligomenorrhoea reflecting an ovulation
  2. Hyperandrogenism (clinical or biochemical with incr free testosterone and decr SHBG)
  3. Polycystic ovaries on USS
Obesity
Acne
Hirsutism
Sub fertility
Oligo or anovulation
199
Q

Criteria for diagnosis of PCOS

SX

A

Rotterdam criteria: 2 of the following

  1. Oligomenorrhoea reflecting an ovulation
  2. Hyperandrogenism (clinical or biochemical with incr free testosterone and decr SHBG)
  3. Polycystic ovaries on USS
Obesity
Acne
Hirsutism
Sub fertility
Oligo or anovulation
200
Q

Management of PCOS

A

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)
201
Q

What additional antenatal care considerations do women pregnant w twins need?

A

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

202
Q

MX of ectopic

A

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

203
Q

Causes of miscarriage

A

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

204
Q

What is adenomyosis

What are risk factors?

A

Endometrial glands found WITHIN myometrium (normal line the outside)

RF: middle aged (30s, 40s)
- multiparous women

205
Q

Causes of abnormal menstrual bleeding

A

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)

206
Q
  1. 2 Types of Dysfunctional uterine bleeding
  2. and underlying pathophys
  3. type of endometrium on histology in each case
A

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
207
Q

DDX intermenstrual bleeding or post coital bleeding

A

Consider local cause

  • polyps
  • infection
  • IUCD
  • uterine or cervical cancer
  • perimenopausal (anovulation)
208
Q

Associated features to ask on history of abnormal bleeding (not including associated features)

A

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)

209
Q

Treatment for abnormal bleeding

A

Treat any underlying causes (e.g.: thyroid)

  1. Medical
    - Anti PGE (NSAIDs, mefanamic acid/ponstan)
    - Tranexamic acid (antifibrinolytic to reduce flow)
    - Hormonal (COCP, depot provera, GnRH analogue)
    - Mirena IUD
  2. Surgical
    - Endometrial ablation (+ tubal ligation)
    - Hysterectomy (+/- oophorectomy)
210
Q

What women are indicated for endometrial ablation

What women shouldn’t this be used on?

A

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
211
Q

What is the most common cause of teenager w menorrhagia?

What are other relatively common causes?

A

Anovulatory dysfunctional uterine bleeding (especially within first 18 months after menarche)

Bleeding disorder (10-20%)
PCOS, thyroid disorder

Pregnancy

Local uterine/cervical causes rare

212
Q

Causes of secondary dysmenorrhoea

A 
Endometriosis
Adenomyosis
Intracavity mass (IUD, polyp, fibroid)
213
Q

MX of endometriosis

A

Do nothing (SX aren’t severe, don’t impact QOL)

Pain relief/analgesia

Hormonal (OCP, progestins, GNRH analogues)

Surgery

  • endometrial ablation or excision
  • hysterectomy
214
Q

Presentation of endometriosis

A

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

215
Q

Mx of adenomyosis

A

Tx is about QOL

Do nothing

Medication

  • Analgesia (NSAIDs)
  • Hormones (OCP, progestin, GNRH analogues)
  • Mirena

Surgical

  • hysterectomy
  • myomectomy
  • ? endometrial ablation
216
Q

Classic presentation (SX and signs) of adenomyosis

A

SX

  • menorrhagia
  • dysmenorrhoea

Signs

  • bulky uterus
  • uterus tender on bimanual palpation
217
Q

Treatment primary dysmenorrhoea

A

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)

218
Q

3 common pathological causes of abnormal vaginal discharge

A
  1. trichomonas vaginalis = trichomoniasis (vaginal itching and irritation + profuse sometimes green frothy discharge)
  2. Candidiasis (severe vulvovaginal irritation assoc w thick cheese discharge)
  3. Bacterial vaginosis (no SX or thin greyish discharge w fishy smell)
219
Q

What is PID? How does it present?

What main organisms cause this?

A

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
220
Q

Causes of PPH

A

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.

221
Q

Investigations and management for suspected adenomyosis

A

USS and MRI (more sensitive)

Mx

  • Hormonal treatment to induce amenorrhoea/reduce flow (IUCD etc, GnRH analogues)
  • Hysterectomy
222
Q

What is adenomyosis

What are risk factors?

A

Endometrial glands found WITHIN myometrium (normal line the outside)

RF: middle aged (30s, 40s)
- multiparous women

223
Q

Mx leiyomyoma

A

Only treat if symptomatic! Mx depends on symptoms

  1. SX-atic treatment can manage heavy/irregular MB (COCP, NSAIDs, tranexamic acid)
  2. Hysteroscopic resection if sub mucous
  3. Myomectomy (remove single specific fibroid)
  4. Embolisation (blood blood supply to single problematic fibroid)
  5. Ablation (U/S beam under MRI guidance destroys fibroid tissue)
  6. Hysterectomy if resistant to treatment
224
Q

Contraception options postpartum

when do you need this from?

A

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)

225
Q

Benefits of breast feeding

A

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

226
Q

Contents of breast milk

A 
Proteins
Ig
Fats (TGL, fatty acids)
Carbs (lactose, galactose, glucose)
Minerals
Electrolytes 
vitamins
water
227
Q

Complications of breast feeding

A

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)

228
Q

Definition and causes of 2dary PPH

A

Significant blood loss 24hours-6 weeks after birth

Causes

  • Infx (endometritis, w GAS, GBS etc)
  • Retained products
229
Q

Sx/signs of endometritis

A 
Postpartum bleeding 
abdominal pain
Malodorous lochia
fever
tachycardia
tender bulky uterus
230
Q

Methods to terminate pregnancy

A

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
231
Q

Features of trisomy 21

A 
low iQ
short stature
congenital abnormalities
Dysmorphic features
Heart and hearing problems
1/2 are FDIU
232
Q

What causes late decelerations?

A

FEtal hypoxia and acidosis, usually due to
reduced uteroplacental blood flow: causes include…

Maternal hypotension
Pre-eclampsia
Uterine hyperstimulation

233
Q

What does sinusoidal CTG pattern indicate?

A

Severe foetal hypoxia
Severe foetal anaemia
Foetal/maternal haemorrhage

234
Q

What are variable decelerations caused by?

A

They are most often seen during labour and in patients’ with reduced amniotic fluid volume.

Variable decelerations are usually caused by umbilical cord compression¹:

235
Q

What do shoulders of deceleration indicate?

A

“shoulders of deceleration“.

Their presence indicates the foetus is not yet hypoxic and is adapting to the reduced blood flow. Reassuring feature

236
Q

What are accelerations?

A

Accelerations are an abrupt increase in baseline heart rate of >15 bpm for >15 seconds.

The presence of accelerations is reassuring.

237
Q

What is normal variability?

what is reduced variability? absent?

A

6-25.
Reduced <=5
Absent <=3

Non reassuring if >45-60min duration

238
Q

What causes reduced variability?

A

Reduced variability caused by:

  1. fetal seeing (last <60min)
  2. maternal sedatives (opiates / benzodiazepines / methyldopa / magnesium sulphate)
  3. Foetal acidosis (due to hypoxia) – more likely if late decelerations are also present
  4. Foetal tachycardia
  5. Prematurity – variability is reduced at earlier gestation (<28 weeks)
  6. Congenital heart abnormalities
239
Q

Causes of prolonged (>2min) severe bradycardia are

A 
Prolonged cord compression
Cord prolapse
Epidural and spinal anaesthesia
Maternal seizures
Rapid foetal descent
240
Q

CTG framework

A

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
241
Q

definition of Small for gestational age and causes

A

<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)
242
Q

Pathophysiology of GDM

How does this lead to fetal macrosomia?

A

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

243
Q

RF for GDM

A 
Age >35yo
FHx
PCOS
Obesity
Previous GDM pregnancy
Certain ethnicities
244
Q

Pathophys of Pre eclampsia

A

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

245
Q

MX of pre-eclampsia

A

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
246
Q

How do you diagnose GDM?

A

Universal 28week 2nd trim screening for all women

  1. OGCT (non-fasting) - if BSL >7.8 -> 2.
  2. OGTT (fasting) - GDM if fasting >=5.5 and/or 2hr BSL >=8
247
Q

Risks of ovulation induction

A 
Multi pregnancy
ovulation hyperstimulation (bloating, nausea, diarrhoea, thirst, decr urine output, abdo pain)
248
Q

Newborn exam

A

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

249
Q

What might an absent red light reflex indicate?

A

Immediate ophthalmology referral as it may suggest congenital cataracts or rarely retinoblastoma

250
Q

Causes of failure to thrive FTT (5)

A
  1. MAY BE PSYCHOSOCIAL so take thorough social hX
    - blunts GH response
  2. Inadequate intake
    - Neglect
    - Low SES
    - Poor diet - micronutrient deficiencies
    - inability to suck/swallow
  3. Inadequate digestion, absorption
    - coeliac
    - CMPA
    - CF
    - pancreatic, cholestatic issue
    - Giardiasis
    - Diabetes
  4. Incr metabolism
    - Carcinoma
    - Hyperthyroid
    - Chronic disease (resp, cardiac, renal, GI)
  5. Prenatal issues
    - prematurity
    - maternal illness/drugs/smoking
    - IUGR
    - chromosomal abnormalities
251
Q

Investigations for short stature/FTT

A

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)

252
Q

MX for short stature

A
  1. education/reassurance
  2. change diet
  3. treat any underlying pathology
  4. +/- GH therapy
  5. psychosocial support
253
Q

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?

A
  1. Familial Short Stature (bone age = chronological age)
    Normal growth vel.
    Normal puberty onset
  2. Congenital Delayed Growth (bone age < chronological age)
    Normal growth vel.
    Delayed puberty
    normal adult height when reached
  3. Pathological (endocrine PICNICS)
    Abnormal growth vel.
254
Q

Pathological causes of delayed growth

A

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)

255
Q

What is the most common haemolytic cause of newborn jaundice?

What is the most severe cause?

A

ABO incompatibility
Mother is usually type O with baby type A

Rh disease is more severe

256
Q

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?

A

Biliary atresia

US of liver/biliary tree to investigate for obstructive causes

Investigate within 6 weeks otherwise results in irreversible liver damage

257
Q

When is newborn jaundice always pathological

A

If it occurs within first 24 hours after birth (suspect haemolysis or sepsis)

Conjugated hyperbilirubinaemia

258
Q

Mx of newborn jaundice

A
  1. Observe/watch
  2. Blue light phototherapy (converts bilirubin into water-soluble form that can be excreted in bile and urine)
  3. 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

259
Q

Causes of pathological vs benign jaundice

A

Benign

  1. Physiological (resolves around 1 week post birth, peaking at 3 days)
  2. Breast milk (peak at 2 weeks)

Pathological
1. Haemolytic

  1. Incr Haem load (haemorrhage, polycythaemia, swallowed blood)
  2. Impaired hepatic uptake and conjugation (Gilbert, hypothyroid, drugs etc)
  3. Mixed (prematurity, sepsis, infants of diabetic mothers, asphyxia)
  4. Structural - biliary atresia
260
Q

Complication of jaundice

A

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)

261
Q

Haemolytic causes of jaundice

A

Immune

  • ABO and Rh blood group incompatibility
  • Drug-induced

Acquired

  • bacterial sepsis
  • congenital intrauterine info

Hereditary

  • G6PD deficiency
  • Hereditary spherocytosis
262
Q

Features ADHD

A

Inattentive
Hyperactive
Impulsive
Poor planning

263
Q

Features of ODD

A

Loses temper
Resistant to authority
Deliberately annoys

264
Q

DC criteria for asthma

A

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

265
Q

Chronic cough ddx and first line inx

A

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

266
Q

Investigations of newborn jaundice

A

FBE + blood firm and reticulocytes
SBR
Indirect and direct Coombs test

267
Q

RF for asthma

A

atopy
Family hx asthma
RSV bronchiolotiis as a child
Exposure to cigarette smoke, allergens, pollution

268
Q

Classifications of asthma and corresponding therapy

A

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
269
Q

Causes of B12 deficiency in kids

+MX

A

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

270
Q

Causes of anaemia

A

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
271
Q

Definition and DDX delayed puberty (boys and girls)

A

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)

272
Q

DDX fevers, rash and refusal to weight bear

A 
JIA
EBV
Osteomyelitis
Septic arthritis
Leukaemia
Lymphoma
SLE 
Osteosarcoma
273
Q

Examples of ACYANOTIC heart defects

A 
1. L->R shunt
VSD
PDA
ASD
AVSD
2. Obstructive heart defects
Pulmonary stenosis
Aortic stenosis
Coarctation of aorta 
Hypoplastic L heart syndrome
274
Q

what are the 2 most common types of CHD in kids?

A
  1. VSD

2. PDA

275
Q

What are SX of heart failure in a newborn?

A

tachypnoea
SOB and sweating when feeding
Failure to thrive
Incr WOB

276
Q

What causes the ductus arterioles to close? when does this occur?

Why might it not close?

A

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
277
Q

What is the treatment for a PDA in a premature infant?

A

Indomethacin or other NSAIDs (inhibit PGE2 to promote ductal constriction and closure)

278
Q

How do PDAs present?

A

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

279
Q

Presentation of a VSD

A

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

  1. 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.

280
Q

What investigations do you do if you hear a murmur in a baby?

A

CXR
ECG
ECHO is diagnostic

281
Q

How do ASDs present?

A

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
282
Q

What is the treatment for ASD and when is it indicated?

A

Indicated if patient has RH enlargement

Transcatheter or surgical closure

283
Q

How does AVSD present?

Tx?

A

Partial AVSD - behaves physiologically and symptomatically like ASD

Complete AVSD - presents like severe VSD (FTT, feeding difficulties, tachypnoea, WOB)

almost always needs surgical closure

284
Q

When does cardiac failure onset in newborns with coarctation of aorta?
How might this present on exam?

A

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

285
Q

Examples of cyanotic heart defects

A

The 4 Ts:

  1. Tetralogy of Fallot
  2. Transposition of great arteries
  3. Tricuspid atresia
  4. Truncus arteriosus
286
Q

What is the tetralogy of fallot and what 4 things comprise it?

A

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
287
Q

Clinical picture of tetralogy of fallot

A

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)

MD3 (7 decks)

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