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Pg 19 Flashcards

1
Q

What are the determinants of the child growth?

A
  • Fetal: 30%; uterine environment
  • Infant: 15%: Nutrition and 3Hs (Health, Happiness, Thyroid Hormones
  • Childhood: 40%: Above + genetics
  • Pubertal: 15%: Sex and thyroid hormones
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2
Q

tanner stages of puberty?

• 1 => 5 (Pre-puberty => Adult)

A

Female breast changes (B)
o B2: Bud.
o B3: Juvenile Smooth contour.
o B4: Areola and papilla above breast.

Pubic hair changes: Male and female (PH)
o PH2: Long, straight
o PH3: Curved and curly
o PH4: Fill out

Male genital stages (G)
o G2: Long penis
o G3: Growth (length and diameter)
o G4: Glans penis and dark scrotal skin

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3
Q

How is bone age assessed and what is its significance?

A

X-Ray of left hand

Predict final height.

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4
Q

How is mid-parental height calculated?

A

Female: MPH = Mean – 7 => Range: +/- 8.5.
Male: MPH = Mean + 7 => Range: +/- 10.

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5
Q

How does puberty differ between males and females?

A
  • First sign is breast bud in females and scrotum > 4 ml in males.
  • Height spurt straight after in females, but 18 months later in males
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6
Q

What is short stature?
• Height is 2 centiles below mean.
Causes?

A 
• Familial
• Constitutional delay
• Pathological: 
o SGA (IUGR, PREM)
o Syndromes (Down, Turner)
o Hormones deficiency (GH, TH deficiency, Steroid excess)
o Health issues (Celiac, CF)
o Happiness
o Nutrients deficiency
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7
Q

extreme short stature?

A

Below 0.4th centile.

SHOX gene deletion on Chr. X

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8
Q

What is disproportionate short stature?

A

Confirm by
o Total height – sitting height = Subischial height.
o Short limbs: Achondroplasia. Short back (Scoliosis and
mucopolysacroidosis).

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9
Q

Hx of a child with short stature

A 
o Growth Centiles
o Familial: Parental height
o Constitutional: FHX delay?
o Pathological:
Pregnancy (GA, IUGR, drugs/ alcohol/ smoking, PREM,
birth weight).
Birth, Development (Child and puberty).
Nutrition: Early feeding problems, weaning, diet now
Health, Hormonal, Happiness
Steroids.
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10
Q

Exam of a child with short stature

A

o Dysmorphic features
o Disproportion
o Disease (Celiac, CF, Crohn’s)
o Development (Tanner).

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11
Q

Investigations of a child with short stature

A 
o Growth charts
o Health:
§ FBC: Anaemia in celiac
§ U+E+ Creatinine: CKD
§ Ca, P, ALP: Bone and kidney
§ ESR, CRP: Crohn’s
§ TTG, EMA: Celiac
o Hormones:
§ TFT
§ GH provocation testes and IGF-1.
§ Dexamethasone suppression test
§ MRI (Craniopharyngioma)
o Karyotype (XO)
o X-rays
§ Bone age
§ Limited skeletal survey (skeletal dysplasia, scoliosis)
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12
Q

Tx of a child with short stature

A

SC GH injections (daily)

IGF-1

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13
Q

tall stature causes?

A
  • Familial
  • Obesity
  • Hormones (Precocious puberty)
  • Syndromes (HCU, Marfan’s)
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14
Q

Microcephaly: < 2nd

causes

A

o Familial: Normal development
o AR condition
o Congenital infection
o Insult (CP)

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15
Q

Macrocephaly: > 98th

causes

A

o Tall stature
o Familial
o Rapidly enlarging = Raised ICP => US (If AF still open) => MRI/CT

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16
Q

Craniocynostosis is the pre-mature fusion of sutures. (Usually do not fuse until late
childhood), resulting in distortion of head shape.

Generalised causes

A

Microcephaly and developmental delay.

Syndromes: Alpert (syndactylyl); exophthalmos (Crouzon)

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17
Q

Craniocynostosis localised causes (more common):

A

Sagittal (most common) => Long flat head
• DDX: Long head of preterm from lying on hard
surface.

Lambdoid:
• Flattening of the skull
• DDX: Plagiocephaly

Coronal:
• Asymmetrical skull

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18
Q

precocious puberty

def

A 
Girls 
Puberty before 8
Benign and common 
pre-mature activation of the HPA axis with very sensitive
ovaries

Boys
Puberty before 9
pathological in boys
Pituitary or adrenal tumour.

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19
Q

precocious puberty
DX

TX

A

DX
Hormonal profile (pituitary and adrenal)
Cranial MRI
Adrenal CT

Tx
Aim at the cause (e.g. Ketoconazole for adrenal causes)
Delay skeletal maturation
Behavioural and psychological

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20
Q

definition and causes of delayed puberty?

A

No puberty by 15 in boys.
Common in boys and usually constitutional: Can give testosterone
injections

No puberty by 14 in girls
Pathological ovaries are very sensitive: Treat underlying cause and induce by estradiol for several months.
o Chromosomal
o Pituitary
o Chronic disease
o Eating disorder
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21
Q

advantages of breast-feeding?

A

Nutrition:
o Easily digested protein curd (Whey: Casein. 60:40).
o Rich in oleic acid, LCFA, and Ca, Fe
o Low solute load

Immune: Decreased infections and hospitalisations
o IgA
o Lysozyme
o Bifidus factors
o Cellular

bonding
Reduce metabolic disease, atopy and maternal cancer.

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22
Q

Introduce solids and wean-off milk at

Off-bottle by

A

6 months

12-18 months

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23
Q

What is weight faltering?

What are its causes?

A

• Sustained drop across 2 centiles or weight below 0.4th.
• Causes: Inadequate food intake
o 90% Non-organic
o 10% organic: (inadequate retention, malabsorption, failure to utilise nutrients, increased requirements)

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24
Q

What are the components of nutritional assessment?

A

Anthropometry: Height, Weight, MUAC < 115 mm.
Labs: Albumin, minerals
Food intake: Recall or diary
Immunodeficiency: Cellular immunity

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25
Q

indications for PN

A

functioning gut,
NG
gastrostomy (if > 6 W). Overnight feeds.

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26
Q

indications for TPN?

A

Bypass gut, PICC or CVC. Monitor for zinc deficiency, blockage, thrombosis and sepsis

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27
Q

definition of severe acute malnutrition
types?
managed?

A
  • Weight -3 Z scores
  • MUAC < 115 mm
  • Kwashiorkor: Protein, Marasmus: Total
Slow frequent feeding: Formula 75 (Carbohydrates)
then Formula (100): Proteins or RUTF
28
Q

rickets
causes,
clinical manifestations, diagnosis

A

Causes: Nutritional, Celiac, Liver, kidney disease.

Manifestations: Seizures, hypotonia, Frontal bossing, Ricketic rosary,
Harrison sulcus, open anterior fontanelle, leg bowing.

DX: Celiac serology, LFT, RFT, dietary history (weaning etc.)
Confirmed by low Ca, P, V.D and high OTH and ALP

29
Q

What is the definition and complications of obesity?

A

• BMI> 98th
• Complications: SUFE, Sleep apnoea, Diabetes, Hyperlipidaemia,
NAFLD, Psychological

30
Q

most common causes of vomiting?

Infants:
Older:

A

Infants: GER, Feeding problems, infection, Food intolerance.

Older: Gastroenteritis, infections, appendicitis, Ulcer

31
Q

red flags for vomiting?

A
  • Bilious => Intestinal obstruction
  • Blood => esophagitis, Intussisiption (Currant jelly stools)
  • Big (Abdomen, Liver): Obstruction, Chronic liver disease.
  • Persistent
  • Projectile => pyloric stenosis
  • Peritonitis => Surgical
  • Cough => Pertussis
  • Dehydration => severe gastroenteritis, DKA, sepsis
  • Faltering growth => Celiac, IBD
32
Q

possible complications of GERD and who is at

risk?

A
  • Faltering growth
  • Aspiration (Recurrent)
  • Esophagitis
  • Sandifer syndrome (GERD+ dystonic neck posturing)

At risk: NM problems and CP

33
Q

What investigations are performed in GERD?

A
  • 24-Oesophageal PH study

* Endoscopy and biopsy

34
Q

How is GERD managed?

A

Food thickeners + Omeprazole

35
Q

What are the clinical features, Dx and Mgt of pyloric stenosis?

A

2-8 week old boy: First in a family with history.
Projectile non-bilious vomiting

Dx: Test Feed =. Visible peristalsis with olive-like mass in the RUQ.
Ass. Hypocholremic hypokalaemic metabolic alkalosis.
Confirm by US

TX: IV fluids and electrolyte correction => Pyloromyotomy (Divide up to but excluding the mucosa).

36
Q

What is infant colic?

A

Inconsolable crying + drawing up of knees and flatus
• Resolves gradually by 3-12 months
• If severe and persistent => Cow ilk protein allergy? => Two-week trial
of protein hydrolysate formula => trial of reflux Tx.

37
Q

DDX of acute abdomen?

A

Surgical: Appendicitis, Obstruction (intussusception and malrotation, inguinal hernia), Peritonitis (Ascites from nephrotic),
Meckle’s diverticulitis, strangulated hernia, ovarian torsion.

Medical: Gastroenteritis, UTI, HSP, IBD, Celiac, constipation, DKA, SCD, pancreatitis

Extra-abdominal: Testicular torsion, Gyne, lower lobe pneumonia

38
Q

clinical features of appendicitis?

A

• Progressive Abdominal pain (made worse by movement), anorexia,
N+V
• Guarding and tenderness at McBurney’s point
• +/- Peritonitis (Generalised guarding)
• +/- RIF mass (Abscess, appendicular mass)
• US: Thick non-compressible appendix with increased flow.

39
Q

clinical features and management of intussusception?

A

• Paroxysmal colicky abdominal pain and pallor+ currant jelly stool+
Sausage–shaped mass on palpation+ Doughnut sign on US.
• Most commonly from foetal impaction => telescoping of ilium into cecum at iliocecal valve. (3 M-2 yrs.), after this age a leading point
(Merkel’s, polyp) more likely.

Tx
Reduction (Radiological by rectal air insufflation unless peritonitis =>
surgical reduction)

40
Q

What is mesenteric appendicitis?

A

Appendicitis mimic, but less severe and often resolve+ URTI

41
Q

clinical features and management of Volvulus?

A

• Twisting of the bowel around its mesentery causing obstruction (Ladd
bands) +/- infarction
• Bilious vomiting in the first days of life
• In children the cause is midgut malrotation, resulting in appendix and
caecum staying in the RUQ.
• DX: Is with Enema: Bird peak sign
• TX: surgical (do not re-rotate but broadens the mesentery with Caecum
and duodenum to left and the DJ on right)+ attachment of bowel to
abdominal wall and appendectomy.

42
Q

recurrent abdominal pain
DEF
DDx

A

3 or more months+ interrupts daily activities.
90% nonorganic,
manifestation of stress

43
Q

recurrent abdominal pain

investigations

A

Urine M+ C&S: Exclude UTI
Abdominal US: Exclude Gallstones and Pelvi-uretric
junction obstruction.
Celiac serology and TFT

44
Q

recurrent abdominal pain

prognosis

A

o Half recover quickly
o Quarter take months
o Quarter remain

45
Q

recurrent abdominal pain

DDx

A

Abdominal migraine
IBS
Ulcer and non-ulcer dyspepsia
Eosinophilic esophagitis

46
Q

Abdominal migraine

A 
o Peri-umbilical pain + headache+ vomiting+ facial pallor lasting
for 2 days
o Long (weeks) symptom-free periods.
o Family or personal HX of migraine
o TX: anti-migraine Meds
47
Q

IBS

A

o Peri-umbilical pain made worse or relieved by defecation
o Bloating
o Alternating bowel habits (Constipation alternating with loose
stool)
o Mucus explosive loose stool
o Feeling go incomplete emptying

48
Q

Ulcer and non-ulcer dyspepsia

A

Pain wakes them at night+ radiate to back.
o FHX of peptic ulcers
o DX: urea breath test, stool antigen => Trial of triple therapy (PPI,
Amoxicillin, clarithromycin) => Endoscopy and biopsy => No
(nodular antral gastritis)=> Functional dyspepsia=> Hypo allergic
diet
o non-ulcer dyspepsia: Early satiety, delayed gastric emptying,
post-prandial vomiting, bloating

49
Q

Eosinophilic esophagitis:

A

o Bolus dysphagia: “Food stuck in upper chest” + Atopy
o Endoscopy: Macroscopically: Linear fissures and
trachealisation.
Micro: Eosinophilic infiltration

50
Q

recurrent abdominal pain

Exclude organic causes

A

Epigastric pain at night +hematemesis (duodenal ulcer)
Dysphagia (esophagitis)
Diahorrea, weight loss, growth failure and bloody stools
(IBD)
Vomiting (pancreatitis)
Jaundice (liver)
Dysuria and secondary enuresis (UTI)
Bilious vomiting and abdominal distension (malrotation)

51
Q

most common cause of gastroenteritis?

A

• Viral: esp. rotavirus.
• C.J (bloody stool)
• Shigella and salmonella (Dysentery: mucus, pus and tenesmus); high
fever in Shigella
• Rapidly dehydrating watery diahorrea: E-coli, cholera

52
Q

Clinical dehydration signs

A

10% of body weight lost. Deteriorating lethargic

child, sunken eyes, tachypnea, tachycardia and reduced skin turgor

53
Q

Shock signs

A

> 10% lost.
Decreased consciousness, sunken Fontanelles,
Increased Capillary refill, weak pulses, hypotension, pale mottled and
cold skin.

54
Q

principles of fluid replacement in gastroenteritis?

A

Oral replacement solution NB
o Contains Na and glucose and help drag water away from lumen.
o Used to prevent and treat
• IV fluids if shock.

o Slowly replace deficit over 24 hr. (100 mls/kg)
o 0.9% Nacl +/- 5% glucose
o Give Maintained fluids
o Encourage oral intake of non-carb fluids
o Monitor electrolytes, Creatinine and glucose

55
Q

types of dehydration?

A

Isonatremic (Most common)
Hyponatremic (Malnutrition); results in seizure and greater shock
Hypernatremia (High fever and hot); Brain shrinkage =results in seizure, altered consciousness, cerebral haemorrhages.
Difficult to recognise.

56
Q

clinical presentation and DDX in malabsorption?

A

Triad: Weight loss + nutrient deficiencies+ abnormal stools

DDX: Celiac, CF, cow’s milk protein allergy, Crohn’s, Short bowel syndrome, Cholestasis liver disease or biliary atresia

57
Q

Celiac disease
clinical features
DX
Tx

A

Classical celiac (Rare): early at 8-24 months with Abdominal pain and distension, steatorrhoea, growth flattering, muscle wasting, irritability

Non-classical: later with anaemia, short stature, abdominal pain and
screening (T1DM)

DX:
o Serology: Anti-endomyseal antibodies and IgA ant TTG.
o Endoscopic biopsy: Lymphocytic infiltrate, villous atrophy and
crypt hyperplasia.

TX: gluten-free diet for life => resolution of symptoms and growth catch up

Complications: Osteopenia and small bowel lymphoma

58
Q

Crohn’s

Presentation:

A

Classical (25%): Abdominal pain, diahorrea and weight
loss
Growth faltering and delayed puberty (may be the only
feature)
Systemic (Lethargy, fever)
Extra-intestinal (Uveitis, mouth ulcers, perianal skin tags
erythema nodosum and arthralgia).

59
Q

Crohn’s DX:

A

Endoscopy (Upper and iliocolonoscopy and biopsy, small bowel imaging= extrainterstinal inflammation). Blood tests
(Anaemia, raised inflammatory markers, low albumin).

60
Q

Crohn’s TX:

A

Remission induction: Nutritional therapy: High protein
modular feeds (75% works) if not => Systemic steroids.
Maintenance: Immunosuppression (Azathioprine or MTX),
biological therapy (Infliximab) , supplemental enteral overnight
feeds (NG or gastrostomy tube).
o Surgery (ilial resection) for complications: Abscess, fistula, and strictures

61
Q

UC Presentation:

A

Pain, diarrhoea, bleeding (less commonly growth

faltering and delayed puberty

62
Q

UC DX:

A

Endoscopy and biopsy

63
Q

UC TX:

A

Mesalasine (induction and maintenance)
o Second line: Immunomodulators, low dose steroids and
biological.
o Severe disease: Admit, IV fluids and steroids => Cyclosporine
o Surgery: Colectomy with ileostomy or iliorectal pouch if
fulminating disease or toxic megacolon.
o Colonoscopy screening for adenocarcinoma (10 years after diagnosis).

64
Q

red flags of constipation?

A
  • Failure to pass meconium in 24 hrs: Hirschsprung.
  • Gross abdominal distension: Hirschsprung.
  • Growth faltering: Celiac, hypothyroidism.
  • Spine lesion: Spina bifida.
  • Lower limb neurology or deformity: Lumbosacral pathology
  • Anal anatomical abnormality
  • Anal bruising: abuse
  • Anal fistula, abscesses: crohn’s
65
Q

management steps of constipation?

A

• Dis-impaction regimen: high dose polyethylene glycol+ electrolytes
• Maintenance: Low dose PEG+ electrolytes +/- Stimulant laxative
(sinna)
• Maintain for 6 months+ encourage fluid intake, dietary changes,
physical activity and good toileting habits

66
Q

Hirschsprung disease diagnosed and managed?

A

• Neonate: Failure to pass meconium + gross abdominal distension.
• Childhood: severe constipation, abdominal distension and growth
failure
• DX: rectal suction biopsy

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