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year 5 specialties key info > PAEDS 4: Upper GI, Lower GI, Inflammatory, Other, Endo > Flashcards

PAEDS 4: Upper GI, Lower GI, Inflammatory, Other, Endo Flashcards

1
Q

What is GORD?

A

Inappropriate relaxation of lower oesophageal sphincter

Most resolve by 12m of age (functional immaturity before then)

However if persistent = GOR disease

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2
Q

How might GORD in a child present?

A

vomiting, refusal to feed/irritability, aspiration chronic cough or wheeze, slow weight gain

important to check onset, duration, feeding behaviour (e.g. positioning), growth

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3
Q

How is GORD investigated?

A

Clinical diagnosis

Maybe consider: 24h LOS pH monitoring, OGD if very serious and no idea what’s going on but unlikely to do anything invasive for this

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4
Q

How is GORD in a child managed?

A

Reassure (common condition) - may be less frequent with time, resolves by 12m

If breastfed:
1st line = breastfeeding assessment
2nd line = consider trial of alginate therapy for 1-2w
3rd line = 4w PPI/H2 antagonist trial e.g. omeprazole/ranitidine

If formula-fed:
1st line = review feeding hx
2nd line = trial smaller, more frequent feeds (150-180mL/kg/day)
3rd line = trial of thickened formula e.g. w/rice starch (enfamil, carabel)
4th line = trial of alginate
5th line = 4w PPI/H2 antagonist

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5
Q

When should referral to a paediatrician be made with a child presenting with GORD?

A

RED FLAGS for same day referral = haematemesis, melaena, dysphagia

CONCERNING FEATURES = faltering growth, unexplained distress, no response to medical therapies, unexplained IDA

COMPLICATIONS = recurrent aspiration pneumonia, dental erosion, unexplained apnoea, recurrent acute otitis media

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6
Q

What is pyloric stenosis?

A

Hypertrophy of pyloric muscle leads to gastric outlet obstruction

Presents age 2-8 weeks

M:F (4:1)

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7
Q

How does pyloric stenosis present?

A

Non-bilious projectile vomiting

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8
Q

What investigations are done for pyloric stenosis?

A

BEDSIDE: examination = palpable mass in RUQ, visible perisistalsis in upper abdomen

BLOODS: hypochloraemic hypokalaemic metabolic acidosis

IMAGING: USS shows target sign

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9
Q

How is pyloric stenosis managed?

A

Fluid resuscitation
Surgery: laparoscopic Ramstedt pyloromyotomy

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10
Q

What is biliary atresia?

A

Progressive fibrosis and obliteration of extra- and intra-hepatic ducts leading to chronic liver failure within 2 years

Very rare: <50 cases/yr in UK

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11
Q

How might biliary atresia present?

A

HISTORY: skin changes (jaundice), stool and urine colours, dehydration, changes in weight or growth

SIGNS: obstructive jaundice (pale stool, dark urine), jaundice, hepatosplenomegaly, faltering growth

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12
Q

What investigations should be done for biliary atresia?

A

BEDSIDE: examination, obs

BLOODS: LFTs, clotting

IMAGING: USS (first line - triangular cord sign), Scintigraphy (Technetium-99), Intraoperative cholangiography/ERCP + biopsy (gold standard)

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13
Q

How is biliary atresia managed?

A

Kasai hepatoportoenterostomy

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14
Q

What is oesophageal atresia?

A

Different types of malformation:

OA = malformation of oesophagus so it doesn’t connect to stomach

TOF = tracheoesophageal fistula - part of oesophagus joined to trachea
- Type C most common
- stomach acid can regurgitate and go into lungs causing CLD/BPD

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15
Q

What is oesophageal atresia assoc. with?

A

polyhydramnios (no swallow), other developmental issues

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16
Q

How might oesophageal atresia present?

A
  • excessive drooling
  • choking
  • failure to swallow or pass an NG tube

HISTORY: pregnancy issues e.g. larger measurements, VACTERL association (vertebral defects, anal atresia, cardiac defects, TOF, renal malformation, limb defects)

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17
Q

How is oesophageal atresia investigated?

A

Prenatal USS

NG tube placement +/- aspirate

Gastrogaffin swallow = gold standard

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18
Q

How is oesophageal atresia managed?

A

Surgical repair - NICU for I&V (intubation and ventilation)
- before: replogle tube (drain saliva from oesophagus)

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19
Q

What is intussusception?

A

Invagination of proximal bowel into distal component

95% ileum through to caecum through ileocaecal valve

Age 3 months to 2 years

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20
Q

What are risk factors for intussusception?

A

Gastroenteritis (viral illness enlarging Peyer’s patches), HSP, CF

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21
Q

How does intussusception present?

A

Abdominal pain, vomit (may be bile stained), red-currant jelly stool (late sign), abdominal distension (+ sausage shaped mass RUQ)

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22
Q

How is intussusception managed?

A

1st line = abdominal USS (target mass)

Alternative = barium (or gastrograffin) enema

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23
Q

How is intussusception managed?

A

Drip and suck:
1st line = rectal air insufflation (otherwise barium/gastrograffin enema)
2nd line (perforation) = surgical reduction w/broad-spectrum abx

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24
Q

What would you do if a child has recurrent intussusception?

A

Consider investigating for a lead point e.g. Meckel’s diverticulum

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25
Q

What is malrotation?

A

Congenital condition in which intestines do not (fully) rotate and fixate in mesentery as usually expected.

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26
Q

What can malrotation lead to?

A

Volvulus - bowel twisting and causing obstruction

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27
Q

What is malrotation associated with?

A

exomphalos, congenital diaphragmatic hernia

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28
Q

How does malrotation present?

A

Abdominal pain and peritonism
Vomiting (bilious)
Bloody stools

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29
Q

How is malrotation investigated?

A

Upper GI contrast study (assess patency)
USS

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30
Q

How is malrotation managed?

A

Urgent laparotomy (Ladd’s procedure)
= untwist volvulus, remove necrotic bowel and place bowel in non-rotation position

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31
Q

What is Hirschsprung’s Disease?

A

Absence of ganglion cells from the myenteric (Auerbach) and submucosal (Meissner’s) plexuses

Begins at the rectum and spreads proximally for a variable distance (75% rectosigmoid), ending at normally innervated, dilated colon

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32
Q

What are RFs for Hirschsprung’s Disease?

A

Down’s
MEN2a
Del(chr10)
Male

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33
Q

How does Hirschsprung’s disease present?

A

Failure to pass meconium <24hrs
Abdo distension
Bilious vomiting
Explosive passage of liquid/foul stools

NOTE: may present later in life w/life-threatening Hirschsprung enterocolitis (C. diff)

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34
Q

How is Hirschsprung’s disease investigated?

A
  • AXR (if obstruction)
  • Contrast (barium) enema = dilated distal segment + narrowed proximal segment
  • Definitive = suction-assisted full-thickness rectal biopsy showing absence of ganglion cells, ACh +ve nerve trunks
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35
Q

How is Hirschsprung’s Disease managed?

A

Initial Mx = bowel irrigation

Followed by = endorectal pull-through (colostomy followed by anastomosing normally innervated bowel)

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36
Q

What is Meconium Ileus?

A

Thick sticky meconium that has a prolonged passing time

Meconium usually passes within 24hrs of delivery, if not, there may be an ileus

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37
Q

What is meconium ileus assoc. with?

A

CF, biliary atresia

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38
Q

How does meconium ileus present?

A

child may vomit meconium instead of passing it as stool

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39
Q

How is meconium ileus managed?

A

abdo exam, heel prick test for CF

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40
Q

How is meconium ileus managed?

A

1st line = gastrografin enema (N-acetylcysteine can also be used)

2nd line = surgery

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41
Q

What is Meckel’s diverticulum?

A

Ileal remnant of vitello-intestinal duct containing ectopic gastric mucosa (i.e. can form gastric ulcers that bleed) or pancreatic tissue

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42
Q

How does meckel’s diverticulum present?

A

Mostly asx
Painless massive PR bleeding
May present w/intussusception, volvulus or diverticulitis

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43
Q

How is meckel’s diverticulum investigated?

A

Technetium scan (increased uptake by gastric mucosa)

Abdominal USS +/- laparoscopy

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44
Q

How is meckel’s diverticulum treated?

A

Only treat if symptomatic

BLEEDING = excision (w/blood transfusion if needed)

OBSTRUCTION = excision of diverticulum and lysis of adhesions

PERFORATION/PERITONITIS = excision or small bowel segmental resection w/perioperative antibiotics

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45
Q

What is a hernia? What are some different types?

A

Hernia = a bulging of an organ or tissue through an abnormal opening

TYPES = indirect inguinal, umbilical, epigastric, femoral

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46
Q

What are some questions to ask in a question about a hernia?

A
  • duration of bulge/lump
  • always vs positional/straining etc.
  • does it retract alone or can they push it back in
  • any pain
  • constipation
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47
Q

How are inguinal hernias investigated?

A

Clinical Diagnosis

EXAMINATION:
- painful vs painless
- cough impulse
- reducible (if not: incarceration)
- auscultation (?bowel sounds)

ESTABLISH DIRECT VS INDIRECT:
1. Locate deep inguinal ring (midway between ASIS and pubic tubercle)
2. Manually reduce hernia
3. Apply pressure over the deep inguinal ring and ask the patient to cough.

If reappears = direct, if not = indirect

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48
Q

What is the different between a direct and indirect inguinal hernia?

A

Direct inguinal hernia = protrusion of abdominal or pelvic contents directly through the posterior wall of the inguinal canal

Indirect inguinal hernia = protrusion of abdominal or pelvic contents into the inguinal canal through the deep inguinal ring

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49
Q

How are inguinal hernias managed?

A

INCARCERATED = emergency surgery

NON-INCARCERATED = elective repair (open or laparoscopic)

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50
Q

How are femoral hernias investigated?

A

Clinical diagnosis

Compared to inguinal hernia:
- femoral = infero-lateral to pubic tubercle
- inguinal = supero-medial to pubic tubercle

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51
Q

How are femoral hernias managed?

A

Surgical management for all of the due to high risk of incarceration

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52
Q

How are umbilical hernias investigated and managed?

A

IX = clinical diagnosis

INCARCERATION = attempt reduction and surgical repair

NON-INCARCERATED =
- large or symptomatic: elective surgical repair (age 2-3yrs)
- small and asx: most self-resolve by age 5. If have not resolved, may consider elective repair

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53
Q

What are risk factors for constipation in children?

A

Low fibre, poor diet, infection, stress/emotional abuse

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54
Q

What questions should be asked in a history for constipation in a child?

A
  • Rule out underlying. conditions e.g. hypothyroidism, CF
  • Rule out red flags e.g. blood in stool
  • diet and lifestyle
  • home and school life
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54
Q

How should constipation be investigated?

A

Clinical diagnosis

AXR for impaction

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55
Q

How is constipation in children managed?

A

DISIMPACTION REGIME:
1. Movicol Paediatric Plain (polyethylene glycol + electrolyte) escalating dose for 2 weeks
2. Add a stimulant laxative (e.g. senna or sodium picosulphate)
NOTE: if movicol not tolerated try stimulant laxative + lactulose/docusate

MAINTENANCE REGIME:
- movicol w/ or w/o stimulant laxative
- dose reduced over period of months

LIFESTYLE & BEHAVIOUR:
- advise behavioural interventions (scheduled toileting, bowel habit diary, reward system)
- diet and lifestyle advice (adequate fluid intake)

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56
Q

What are the different types of laxatives?

A

Bulk-forming = fybogel, methylcellulose

Osmotic = lactulose, movicol

Stimulant = bisacodyl, senna, sodium picosulphate

Stool softeners = arachis oil, docusate sodium

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57
Q

What is Crohn’s disease?

A

Affects any part of GI tract mouth to anus

Transmural inflammation most commonly affecting distal ileum and proximal colon

58
Q

How does Crohn’s disease present?

A
  • abdo pain, diarrhoea, weight loss
  • fever, lethargy
  • aphthous ulcers, perianal skin tags
  • growth failure, delayed puberty
  • uveitis, arthralgia, erythema nodosum
  • complications: strictures and fistulae
59
Q

How is Crohn’s disease investigated?

A

BEDSIDE: Abdo exam, assess impact on daily functioning, risk of osteoporosis

BLOODS: faecal calprotectin, FBC (iron, B12, folate), CRP, ESR

IMAGING: upper GI and small bowel contrast scan, colonoscopy and biopsy (cobblestones, non-caseating granulomas)

60
Q

How is Crohn’s disease managed?

A

INDUCE REMISSION:
- pharmacological mx = steroids (prednisolone)
- nutritional mx = replace diet w/whole protein modular diet (excessively liquid 6-8w), may need NG if child struggles to drink that amount, products easily digested, provide all nutrients needed to replace weight loss

MAINTAINING REMISSION:
- aminosalicylates (e.g. mesalazine)
- immunosuppressive drugs (azathioprine, methotrexate, mercaptopurine): no live vaccines but need pneumococcal + flu vaccine
- anti-TNF antibodies in biologic therapies (e.g. infliximab)

MONITORING: ferritin, B12, calcium and vitamins

COMPLICATIONS: Consider surgery for complications e.g. obstruction, fistula, abscess, severe localised disease

SUPPORT: Crohn’s and Colitis UK info and leaflets

61
Q

What is Ulcerative Colitis?

A

Partial thickness inflammation, distal to proximal pattern, crypt damage and ulceration

62
Q

What is ulcerative colitis associated with?

A

PSC, toxic megacolon, enteric arthritis, haemorrhage, bowel cancer

63
Q

How does ulcerative colitis present?

A
  • rectal bleeding, diarrhoea, abdominal pain
  • weight loss and growth failure
  • erythema nodosum, arthritis
64
Q

How is ulcerative colitis investigated?

A

Same ix as Crohn’s disease

IMAGING: endoscopy (confluent colitis extending from rectum proximally, histology = mucosal inflammation/ulceration, crypt damage)

GRADING SEVERITY:
- Paediatric Ulcerative Colitis Activity Index (PUCAI) - be aware of coexistent depression
- Truelove and Witts Score

65
Q

How is ulcerative colitis managed?

A

1st LINE = topical aminosalicylates
- used to maintain remission
- no improvement in 4w, move to oral, then to 2nd line
- can use oral azathioprine or mercaptopurine if aminosalicylates insufficient

2nd LINE = topical or oral corticosteroids if aminosalicylates not tolerated/contraindicated e.g. prednisolone, beclomethasone

3rd LINE = oral tacrolimus

4th LINE = biological agents (infliximab, adalimumab and golimumab)

5th LINE (resistant disease) = surgery (colectomy w/ileostomy or ileojejunal pouch)

MEDICAL EDUCATION: UC assoc. w/ increased risk of bowel cancer, regular screening performed after 10yrs of diagnosis

SUPPORT: Crohn’s and Colitis UK

66
Q

How is severe fulminating disease in UC managed?

A

EMERGENCY

MDT approach
IV corticosteroids or ciclosporin and assess likelihood of needing surgery
- >8 stools/day
- pyrexia
- tachycardia
- AXR w/colonic dilatation
- low alb, Hb
- high PLTs or CRP

Consider IV cicosplorin (if IV corticosteroids contraindicated or ineffective)

67
Q

What is Coeliac Disease?

A
  • autoimmunity to gliadin (in gluten, wheat, barley and rye, shorter villi and flat mucosa)
  • common
  • HLA-DQ2 (95%) and DQ8 (80%) association
68
Q

How does coeliac disease present?

A
  • malabsorption syndrome = failure to thrive, abdo distension, bloating, irritability
  • malnutrition = wasted buttocks, distended abdo
  • dermatitis herpetiformis (itchy papulovesicular rash on elbows or knee)
69
Q

How is coeliac disease investigated?

A

Serological diagnosis:
- IgA anti-TTG = most sensitive
- IgA anti-endomysial cell antibodies = less sensitive

NOTE: if IgA deficient use IgG DGP

BLOODS: FBC, blood smear (IDA, vit B12/folate deficiency, vit D)

Confirm diagnosis via grading w/’Marsh’ system (for adults + older children) = OGD + jejunal biopsy (villous atrophy, crypt hyperplasia, increased IELs)

70
Q

How is coeliac disease managed?

A

DIET: remove all products containing wheat, rye and barley

MDT: dietician, child psychologist, school involvement, GP, gastroenterologist

Dietician referral if problems adhering to diet

REVIEW: annual (6-12m) reviews checking height + weight, r/v sx, diet, consider bloods

SUPPORT: Coeliac UK

71
Q

What can non-adherence to dietary management of coeliac disease lead to?

A
  • micronutrient deficiency
  • osteoporosis
  • EATL (enteropathy-associated T lymphoma)
  • hyposplenism
72
Q

What is Cow’s milk protein allergy?

A

IgE mediated or delayed reaction to cow’s milk protein

Usually presents in first 3m of life in formula-fed children

Breastfed infants can still get a reaction from proteins that mother eats passing to breast milk

73
Q

How does cow’s milk protein allergy present?

A

“3m old baby that vomits and has diarrhoea after every

IgE mediated = urticaria, angioedema, rash, erythema, N&V, diarrhoea, abdo pain, sneezing, anaphylaxis, wheezing etc.

Non-IgE mediated = erythema, atopic eczema, GORD, change in frequency of stools, blood/mucus in stools, abdominal pain, FTT, infantile colic, constipation, food aversion, pallor

74
Q

How is cow’s milk protein allergy investigated?

A
  1. Skin prick allergy testing OR
  2. measurement of specific IgE antibodies (RAST)

Referral to specialist if:
- faltering growth with >1 GI sx of allergy
- >1 acute systemic or severe delayed reactions
- severe atopic eczema
- persisting suspicion
- multiple allergies

75
Q

How is cow’s milk protein allergy managed?

A

Referral if indicated, otherwise:

1st LINE = trial cows’ milk elimination for 2-6w
- breastfed = mum to exclude cow’s milk protein from diet (consider 1g Ca and 10mcg vit D supplementation) (2-3w for cow’s milk to be fully eliminated from breastmilk)
- formula-fed = hypoallergenic infant formula (e.g. extensively hydrolysed or amino acid formula if severe)
- weaned/older child = exclude cows milk protein from their diet

2nd = monitor growth, nutritional counselling w/paediatric dietician

3rd = re-evaluate tolerance to cow’s milk protein every 6-12m
- reintroduce, if tolerance established use milk ladder to gradually increase exposure to less processed milk

76
Q

What is appendicitis?

A

Most common cause of abdo pain in childhood (rare if <3yo)

Faecolith (stony mass of compacted faeces) more common in pre-school children and perforation more common

77
Q

How does appendicitis present?

A
  • anorexia, N&V
  • umbilical to RIF pain
  • fever, tenderness etc.
78
Q

How is appendicitis investigated?

A

BEDSIDE: clinical diagnosis, watchful waiting observation + examination

BLOODS: FBC, pregnancy test if female, CRP

IMAGING: consider USS if diagnostic uncertainty

79
Q

How is appendicitis managed?

A

GAME:
G = group and save
A = antibiotics, IV
M = MRSA screen
E = no Eating, must be NBM

Surgery = appendectomy (definitive mx)

80
Q

What is mesenteric adenitis?

A

Mainly in children <15yo after a recent viral/bacterial infection (inc. UTIs)

Common cause of abdominal pain

81
Q

How does mesenteric adenitis present?

A

abdominal pain - central or RIF
may have nausea +/- diarrhoea
decreased appetite

82
Q

How is mesenteric adenitis investigated?

A

Clinical diagnosis

Bloods to exclude appendicitis (bloods, urine MC&S, USS)

Large mesenteric lymph nodes seen at laparoscopy (w/normal appendix) = definitive Ix but never done

83
Q

How is mesenteric adenitis managed?

A

Simple analgesia (sx usually resolve in a few days, max. 2w)

Safety net for increased pain or deterioration

84
Q

What is necrotising enterocolitis?

A

Most common surgical emergency in newborn babies - tends to affect premature babies and LBW

Immature/fragile bowels leads to poor blood flow and infection of intestines

Often begins after starting enteral feeding

85
Q

How does necrotising enterocolitis present?

A

Early Sx = biliary vomiting, feed intolerance

Abdo distension

Blood-stained stool

Rapid deterioration and shock

86
Q

How is necrotising enterocolitis investigated?

A

BLOODS: blood cultures

IMAGING: AXR - ‘gas cysts’ in bowel wall, distended loops, thickened walls

87
Q

How is necrotising enterocolitis managed?

A

Bowel rest - switch to parenteral nutrition and stop oral feed

Broad-spectrum antibiotics - cefotaxime/tazocin and vancomycin
- stage IA/IB = 3/7d
- stage IIA = 7-10d
- stage IIB, III = 14d

Laparotomy if perforation

88
Q

What are long term consequences of necrotising enterocolitis?

A

20% mortality/morbidity acutely

development of strictures

malabsorption (if extensive bowel resection is necessary)

89
Q

What are threadworms?

A

Infect bowel, lay eggs near rectum, itchiness, scratching leads to contamination of fingers, transmission

90
Q

How do threadworms present?

A

itchiness in anal/perianal region

91
Q

How are threadworms investigated?

A

Clinical diagnosis

Stool sample (ova, cysts, parasites)

92
Q

How are threadworms managed?

A

Single dose mebendazole for whole household
- repeat after 2w if persistent sx
- rigorous hygiene for 2w if on mebendazole or 6w if hygiene measures alone (handwashing, cutting fingernails, showering everyday, changing bedding + nightwear, dust and vacuum)
- NO exclusion from school
- <6m treat w/just hygiene for 6w

93
Q

What is Toddler’s Diarrhoea?

A

chronic and non-specific diarrhoea

commonest cause of loose stools in preschool kids

underlying maturational delay in intestinal mobility - increased intestinal hurry (not malabsorption)

94
Q

How does toddler’s diarrhoea present?

A
  • varying consistency stools (well-formed to explosive and loose +/- presence of undigested veg)
  • child well and thriving w/no precipitating dietary factors and normal examination)
95
Q

How is toddler’s diarrhoea investigated and managed?

A

Clinical diagnosis

Mx = reassurance, safety net on red flags

96
Q

What is infantile colic?

A

Common symptom complex in infants that generally resolves by 3-12 months

97
Q

How does infantile colic present?

A

Manifests as random inconsolable crying and drawing up of hands and feet

98
Q

How is infantile colic investigated and managed?

A

Clinical diagnosis

Mx = reassurance and safety net on red flags

99
Q

What is puberty determined by for females and males?

A

Females = breast development (Tanner’s 5 breast development stages)

Males = testicular development >4mL (Prader’s orchidometer)

100
Q

At what age would a child be classed as having undergone precocious puberty?

A

Girls = age <8yo

Boys = age <9yo

101
Q

What are the 3 big overarching causes of precocious puberty?

A
  1. Gonadotrophin-dependent precocious puberty (GDPP)
  2. Gonadotrophin-independent precocious puberty (GIPP) - 20% of PP
  3. Benign isolated precocious puberty (generally self-limiting)
102
Q

What are the GDPP causes?

A
  • premature activation of HPG axis
  • idiopathic
  • CNS abnormalities (tumours, trauma, central congenital disorders)
103
Q

What are the GIPP causes?

A

Early puberty from increased gonadal activation dependent of HPG

OVARIAN = follicular cyst, granulosa cell tumour, Leydig cell tumour, gonadoblastoma

TESTICULAR = Leydig cell tumour, testotoxicosis (familial, defective LH-R function)

ADRENAL = congenital adrenal hyperplasia, Cushing’s

TUMOURS = b-hCG secreting tumour of liver, ovary, testes, adrenal

McCune-Albright syndrome = multiple endocrinopathy of thyrotoxicosis, Cushing’s, acromegaly (S/S = polyostotic fibrous dysplasia, cafe-au-lait spots, ovarian cysts)

EXOGENOUS HORMONES = COCP, testosterone gels

104
Q

What are causes of benign isolated precocious puberty?

A

PREMATURE THELARCHE = isolated breast development before 8yo, from maternal oestrogen
- Sx = absence of other pubertal signs, normal growth, normal USS of uterus, rarely progress past Tanner stage 3

PREMATURE PUBARCHE/ADRENARCHE = isolated pubic hair development before 8yo in girls or 9yo in boys
- early adrenal androgen secretion in middle childhood
- more common Asian/Afro-Caribbean

PREMATURE MENARCHE = isolated vaginal bleeding before 8yo

105
Q

How is precocious puberty investigated?

A

GOLD STANDARD = GnRH stimulation test
- FSH, LH low = GIPP
- FSH, LH high = GDPP
Wrist XR (non-dominant) for skeletal age
General hormone profile (basal LH/FSH, serum testosterone and oestrogen)
Urinary 17-OH progesterone if CAH suspected

FEMALES = not normally of concern
- pelvic USS
- premature onset of normal puberty: multicystic ovaries and enlarging uterus
- r/o gonadal tumour, cysts

MALES = most commonly organic cause
- Prader’s orchidometer measurement and testes exam (bilateral enlargement = GDPP ?intracranial lesion, MRI; unilateral enlargement = gonadal tumour; small = tumour or CAH)

106
Q

How is precocious puberty managed?

A

Refer to paediatric endocrinologist

If GDPP w/no underlying pathology = no treatment required

GDPP
- GnRH agonist (e.g. leuprolide) + GH therapy
- DnHR agonist + cryproterone (anti-androgen)

GIPP
McCune Albright or Testotoxicosis
- 1st line = ketoconazole or cyproterone
- 2nd line = aromatase inhibitors
CAH: hydrocortisone + GnRH agonist

107
Q

What is adrenal insufficiency/congenital adrenal hyperplasia?

A

Most common non-iatrogenic cause of low cortisol

Multiple forms of CAH - most common = 21-hydroxylase deficiency

Autosomal recessive

108
Q

How does adrenal insufficiency/CAH present?

A
  • Virilisation of external genitalia (F = clitoromegaly, fusion of labia, M = enlarged genitals, pigmented scrotum)
  • Salt-losing crisis (often 1st sign in M) = vomiting, weight loss, hypotonia, circulatory collapse
  • Tall stature
  • excess androgens = muscular build, adult body odour, pubic hair, acne
109
Q

How is adrenal insufficiency/CAH investigated?

A

Initial Ix for ambiguous genitalia, no external gonads = USS to examine internal genitalia

Confirmatory for CAH = raised plasma 17a-hydroxyprogesterone (unable to do in newborn)
- for newborn 1st Ix = USS

Biochemical abnormalities in FBC:
- salt-losing crisis = low Na+, high K+
- metabolic acidosis = low bicarb
- hypoglycaemia (low glucose from low cortisol)

Other confirming tests = karyotyping, high urea (dehydrated), b-hCG

110
Q

Why are the different types of adrenal insufficiency/CAH?

A
  • 5-alpha-reductase deficiency
  • androgen insensitivity syndrome
  • 21-hydroxylase deficiency (CAH)
  • 17-alpha-hydroxylase deficiency (CAH)
111
Q

How does 5-alpha reductase deficiency present?

A

ambiguous genitalia but internal male organs present, XY genotypes, increased testosterone at puberty virilising so get “penis-at-12” syndrome

112
Q

How does androgen insensitivity syndrome present?

A

feminisation, no internal male or female organs, XY genotype

113
Q

How does 21-hydroxylase deficiency present?

A

ambiguous genitalia, salt losing crisis, XX genotype

114
Q

How does 17-alpha-hydroxylase deficiency present?

A

feminisation, hypertensive, XY genotype

115
Q

How is adrenal insufficiency/CAH managed?

A

Corrective surgery = for affected females on the external genitalia
- F are raised as F
- definitive surgery often delayed until early puberty

Long-term Mx
- lifelong glucocorticoids (hydrocortisone) to suppress ACTH + testosterone
- mineralocorticoids (fludrocortisone) if salt loss
- monitor growth, skeletal maturity, plasma androgens and 17-alpha-hydroxyprogesterone levels
- additional hormone replacement at times of illness or surgery i.e. double hydrocortisone

Salt-losing crisis = IV hydrocortisone, IV saline, IV dextrose

116
Q

What is androgen insufficiency syndrome?

A

Delayed puberty in a ‘girl’ w/bilateral groin swellings (undescended testes)

Genotype = XY, phenotype = XX

Can be complete or partial:
- COMPLETE = testosterone no effect, genitals entirely female
- PARTIAL = testosterone has some effect, genitals more ambiguous

117
Q

How does androgen insufficiency syndrome present?

A
  • ambiguous genitalia from birth
  • undescended testes
  • often diagnosed at puberty (girl w/CAIS will develop breasts, may be slightly taller than usual, not have periods, little to no pubic hair)
118
Q

How is androgen insufficiency syndrome investigated?

A

BEDSIDE = abdo exam, external genitalia exam

BLOODS = oestrogen/progesterone, testosterone

SPECIAL TESTS = karyotype

119
Q

How is androgen insufficiency syndrome managed?

A

-MDT approach
- Counselling
- Surgery e.g. removing undescended testicles, vaginal dilatation, breast reduction etc.
- Hormone replacement e.g. encouraging puberty, preventing menopausal sx and osteoporosis (if testicles removed)

120
Q

What is growth hormone deficiency?

A
  • variety of mutations exist, some sporadic and some familial
  • rare
121
Q

How does growth hormone deficiency present?

A

short stature, poor growth, absent growth spurt/delayed puberty

122
Q

How is growth hormone deficiency investigated?

A

BEDSIDE: Examination (plot growth chart)

BLOODS: TFTs, IGF-1, baseline pituitary hormones

SPECIAL TEST: GH provocation test e.g. insulin, glucagon, arginine

IMAGING: Wrist XR for bone maturity

123
Q

How is growth hormone deficiency managed?

A

GH replacement therapy

124
Q

What is congenital hypothyroidism?

A

Assoc. w/irreversible neurological problems and poor growth if untreated

Number of causes:
- thyroid gland defects (most common) = not inherited
- disorder of thyroid hormone metabolism = inherited
- hypothalamic or pituitary dysfunction
- transient hypothyroidism due to maternal meds or antibodies

125
Q

How does congenital hypothyroidism present?

A
  • feeding difficulties, lethargy, constipation
  • large fontanelles, myxoedema, nasal obstruction, low temp, jaundice, hypotonia, pleural effusion, short stature, oedema +/- goitre, +/- congenital defects
  • unique sx = coarse features, macroglossia, umbilical hernia
126
Q

How is congenital hypothyroidism investigated?

A
  • high TSH, low T4
  • measure thyroid autoantibodies +/- US or radionucleotide scan
127
Q

How is congenital hypothyroidism managed?

A

Early detection + replacement
- levothyroxine OD, titrate dose to TFTs + regular monitoring
- monitor growth, developmental milestones

128
Q

What is T1DM?

A

autoimmune destruction of beta cells of pancreas

assoc. w/HLA-DR and HLA-DQ

129
Q

How does T1DM present?

A

Weight loss
Polyuria and polydipsia
Hyperglycaemia
Recent infections
Bedwetting
PMHx and FHx of autoimmunity

130
Q

How is T1DM investigated?

A
  • random plasma glucose >11.1
  • 2h plasma glucose >11.1
  • fasting plasma glucose >7
  • HbA1c >48mmol/mol / >6.5%
131
Q

How is T1DM managed?

A

MDT = paediatrician, PDSN, psychologist, school, GP

1st LINE = multiple daily injection basal-bolus
- injections of short-acting insulin before meals, w/1 or more separate daily injections of intermediate acting insulin or long acting insulin analogue

2nd LINE = continuous SC insulin infusion (insulin pump)
- programmable pump/insulin storage device that gives regular or continuous amounts of insulin (usually rapid-acting insulin or short-acting insulin)

EDUCATION:
- insulin injection method and sites
- blood glucose prick monitoring = >5 capillary blood glucose/day, ongoing monitoring for children w/frequent severe hypoglycaemia, impaired awareness, inability to recognise/relay sx of hypoglycaemia
- HbA1c checked 4x / yr
- healthy diet and exercise (DAFNE)

MONITORING:
- annually from 12yo for diabetic retinopathy, nephropathy and HTN

SAFETY NETTING: Sick day rules
- explain sx of DKA
- check blood ketones when ill or hyperglycaemic
- recognition and treatment of hypoglycaemia

132
Q

What are the different types of insulin?

A

Long acting = glargine, determir

Short acting = lispro, glulisine, aspart

133
Q

What are the BSPED guidelines for DKA?

A

DIAGNOSIS:
- BM >11.1
- ketones >3
- pH <7.3 or bicarb <15

SEVERITY:
- Mild = pH <7.3 = 5% fluid deficit
- Moderate = pH <7.2 = 7% fluid deficit
- Severe = pH <7.1 = 10% deficit

134
Q

What should be monitored in a child w/DKA?

A

Monitoring every hour (30mins if severe DKA, or <2yo)

HOURLY = CBG, obs, fluid balance (input/output), GCS, ECG

2hrs, then 4hrs = glucose, U&Es, CBG, ketones

135
Q

What are the rough steps to treating DKA?

A
  1. Emergency management A-E
  2. Fluid management
  3. Insulin/dextrose therapy after 1-2 hrs of IV fluid replacement
136
Q

What is the emergency management of DKA?

A

ABCDE

Shocked = 20mL/kg bolus over 15 mins + 10mL/kg bolus if required w/max 40mL/kg

Not shocked = 10mL/kg bolus over 60 mins

Ix = blood glucose, FBC, U&Es, blood gas, ketones, full clinical assessment inc. GCS

137
Q

What is the fluid management of DKA?

A
  1. DEFICIT = (deficit x weight x 10) - initial bolus if non-shocked - replace over 48hrs
  2. MAINTENANCE (remove initial bolus if not shocked)
    - 1st 10kg = 100mL/kg/day
    - 2nd 10kg = 50mL/kg/day
    - every kg >20kg = +20mL/kg/day
  3. ADDITIONAL ELECTROLYTES - ensure 20mmol KCl per 500mL saline (i.e. 40mmol per L), unless K+ raised
138
Q

What is the insulin/dextrose therapy management of DKA?

A

Insulin dose = IV 0.05-0.1 units/kg/hr
- start dextrose when <14mmol/L
- change to SC insulin once resolving (30min before stopping IV)
- place on ECG monitor to identify hypokalaemia

139
Q

What are potential complications of DKA?

A
  • cerebral oedema (rx w/mannitol or hypertonic saline, restrict fluids)
  • hypokalaemia (rx by stopping insulin temporary)
  • thrombosis (rx w/heparin prophylaxis)
  • aspiration pneumonia
  • inadequate resuscitation
140
Q

How is obesity in children classified?

A

Using centiles

OVERWEIGHT = 85-94th centile
OBESE = >95th centile
SEVERELY OBESE = 99th centile

141
Q

What are RFs for obesity in children?

A

Low SES, poor diet, genetics, little exercise

142
Q

How is obesity investigated?

A

BEDSIDE: growth chart plotting, nutritional assessment (triceps skinfold thickness)

BLOODS: cholesterol, triglyceride levels, endocrine assays

URINE: glucosuria, T2DM

RADIOLOGY: USS/CT/MRI head for specific conditions or syndromes

143
Q

How is obesity managed?

A

CONSERVATIVE:
- self esteem and confidence building (early intervention is key)
- address lifestyle

THERAPEUTIC AIMS:
- reduce excess weight whilst not compromising growth
- dietary counselling
- behaviour modification (age-dependent approach)
- stepwise physical activity programme
- adherence to plan needs strong family support

NOTE: surgery not recommended in young people

year 5 specialties key info (16 decks)

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