Gastroenterology and paeds surgery Flashcards

1
Q

What is the presentation of constipation in children?

A

(reduced freq of stool compared to normal)
- < 3 stools a week
- Hard stools, rabbit dropping, difficult and painful to pass
- Abdo pain, can palpate stool in abdo
- Retentive posturing - standing/sitting w straight stiff legs, voluntarily holding in stool
- Rectal bleeding
- Faecal impaction = overflow soiling
- Encopresis

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2
Q

What is encopresis?

A
  • Faecal incontinence, not pathological until 4 years old
  • Sign of chronic constipation = rectum becomes stretched and looses sensation
  • Large hard stools remaain in rectum and loose stools leak out = soiling
  • Other causes - Hirschprung’s, ID, cerebral palsy, stress and abuse
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3
Q

What are lifestyle factors contributing to constipation?

A
  • Habitually not opening bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial probs - difficult home or school environment
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4
Q

What are secondary causes of constipation?

A
  • Hirschsprung’s
  • Cystic fibrosis, esp meconium ileus
  • Hypothyroidism, hypocalcaemia, coeliac disease
  • Spinal cord lesions
  • Sexual abuse
  • Intestinal obstruction
  • Anal stenosis
  • Cows milk intolerance
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5
Q

What are the red flags in constipation?

A
  • Not passing meconium w/i 48 hours of birth = CF or Hirschsprung’s
  • Neuro signs, esp in lower limbs
  • Vomiting - bowel obstruction and Hirschsprung’s
  • Ribbon stool - anal stenosis
  • Abnormal anus = IBD, anal stenosis, sexual abuse
  • Abnormal lower back or buttocks - spina bifida, sacral agenesis
  • Failure to thrive - Coeliac, hypothyroid
  • Acute severe abdo pain and bloat - obstruction or intussusception
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6
Q

What are some complications of constipation?

A
  • Pain
  • Reduced sensation
  • Anal fissures
  • Overflow and soiling
  • Psychosocial morbidity
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7
Q

What is the management of idiopathic constipation?

A
  • Correct reversible factors - high fibre diet and good hydration
  • Start laxatives - movicol 1st line - long term and slowly weaned off
  • Faecal impaction = disimpaction regimen w high doses of laxatives - at first osmotic laxative, then stimulant if not tolerated
  • Encourage and praise visiting the toilet - scheduling visits, bowel diary and star charts
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8
Q

How do you diagnose Hirschsprung’s disease?

A
  • Usually presents w delay in meconium and failure to thrive so normally in 1st month but can present late rarely
  • Rectal biopsy = gold standard
  • Barium enema
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9
Q

What is Coeliac disease?

A

Autoimmune condition where gluten exposure causes inflam of small bowel, esp jejunum due to autoab attacking epithelial cells. Causes atrophy of intestinal villi = malabsorption of nutrients and disease related sx.

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10
Q

What are the ab and genetic associations in Coeliac disease?

A

Anti TTG and anti EMA - increase w more active disease and disappear w effective treatment
HLA-DQ2 and HLA-DQ8 (don’t know if need to know)
Always test new T1DM diagnosis for coeliac disease even if don’t have sx.

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11
Q

What is the presentation of coeliac disease?

A
  • Can be asymptomatic
  • Failure to thrive in young children
  • Diarrhoea or steatorrhoea
  • Fatigue, weight loss, mouth ulcers
  • Secondary iron, B12 or folate deficiency anaemia
  • Dermatitis herpetiformis - itchy blistery skin on abdo
  • Abdo distension, short statue and wasted buttocks
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12
Q

What neurological sx can coeliac disease present with?

A
  • Peripheral neuropathy
  • Cerebellar ataxia
  • Epilepsy
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13
Q

What are the ix into Coeliac disease?

A
  • Need to still be on gluten inclusive diet while ix
  • Basic bloods - FBC, U+E, LFT, iron, B12, folate
  • Total immunoglobulin A levels to exclude IgA def
  • Check for ab - serology
  • OGD and intestinal biopsy - crypt hypertrophy, villous atrophy, intra epithelial lymphocytes
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14
Q

What are the complications of coeliac disease?

A
  • Vit deficiency, anaemia, OP
  • Ulcerative jejunitis
  • Enteropathy associated T cell lymphoma of the intestine EATL
  • Non Hodgkin lymphoma
  • Small bowel adenocarcinoma but rare
  • Hyposplenism
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15
Q

What is the treatment of coeliac disease?

A

Life long GF diet

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16
Q

What is the presentation of GORD in children?

A
  • Chronic cough/hoarse cry
  • Distress, crying or unsettled after feeding - normal for babies to have some reflux after larger feeds but is a problem when they are distressed
  • Reluctance to feed
  • Pneumonia
  • Poor weight gain
  • Retrosternal or epigastric pain may be reported
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17
Q

What are some differentials for vomiting in children?

A
  • Overfeeding
  • GORD
  • Pyloric stenosis - projective vomiting
  • Gastritis and gastroenteritis
  • Appendicitis
  • Infections - UTI, tonsilitis, meningitis
  • Intestinal obstruction
  • Bulimia
  • Upper GI bleed
  • Raised ICP
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18
Q

What are some red flags for vomiting?

A
  • Not keeping down feed or forceful vom - pyloric stenosis or bowel obstruction
  • Bile stained vomit - bowel obstruction
  • Haematemesis or malaena
  • Abdo distension
  • Reduced conc, bulging fontanelle, neuro signs - raised ICP or meningitis
  • Resp sx - aspiration pneumonia
  • Blood in stools - gastro or cows milk allergy
  • Signs of infection
  • Rash, angioedema
  • Apnoea - v concerning
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19
Q

What is apnoea?

A

Muscles and soft tissues of throat collapse causing total blockage of the airway for more than 10 secs

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20
Q

What is the management of GORD?

A

Simple - small freq meals, burp reg, don’t over feed, keep baby upright after feeding
Problematic - gaviscon mixed w water after feeds for a 2 week trial, thickened milk or formula, PPI when doesn’t work gaviscon doesn’t work
Severe - need to ix further = barium meal and endoscopy, surgical fundoplication

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21
Q

What are some complications of GORD in children?

A
  • Reflux oesophagitis
  • Recurrent aspiration pneumonia
  • Recurrent acute otitis media
  • Dental erosion
  • Apnoea
  • Apparent life threatening events
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22
Q

What is Sandifer’s syndrome?

A

Brief eps of abnormal movements associated w GORD:
- Torticollis - forceful contraction of neck muscles = neck twisting
- Dystonia - arching of back or unusual posture
Resolves as reflux improves.

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23
Q

What are some medical differentials for abdo pain in children?

A
  • Constipation
  • UTI
  • Coeliac disease
  • IBD and IBS
  • Mesenteric adenitis
  • Abdo migraine
  • Pyelonephritis
  • Henoch Schonlein purpura
  • Tonsilitis
  • Diabetic ketoacidosis
  • Infantile colic
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24
Q

What are some surgical differentials for abdo pain?

A
  • Appendicitis
  • Intussusception
  • Bowel obstruction
  • Testicular torsion
  • Ectopic
  • Ovarian torsion and cyst rupture
  • Meckel’s diverticulitis
  • Pancreatitis
  • Mesenteric adenitis
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25
Q

What are red flags for abdo pain?

A
  • Persistent or bilious vom
  • Severe chronic diarrhoea
  • Fever
  • Rectal bleeding
  • Weight loss or faltering growth
  • Dysphagia
  • Nighttime pain
  • Abdo tenderness
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26
Q

What is recurrent abdo pain?

A

Repeated episodes of abdo pain w/o a cause - non organic/functional. Overlaps w functional abdo pain and IBS.
Often corresponds to stressful life events eg. bereavement of bullying.

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27
Q

What is the management for functional GI disorders?

A
  • Explanation and reassurance
  • Distraction from pain and don’t ask about it
  • Sleep, reg meals, healthy balanced diet, stay hydrated, exercise, reduce stress
  • Probiotic supplements
  • Avoid NSAIDs
  • Address psychosocial triggers and support
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28
Q

What is abdo migraine?

A

Central abdo pain lasting >1 hour w normal examination, can get associated N+V, anorexia, pallor, headache, photophobia, aura

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29
Q

What is the management of abdo migraine?

A

Treat acute attack - low stimulus environment, paracetamol, ibuprofen, sumatriptan
Preventative - pizotifen, propanolol, cyproheptadine, flunarazine

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30
Q

What are the features of Crohn’s?

A

crows NESTS
No blood or mucus (less common in Crohns)
Entire GI tract
Skip lesions
Terminal ileum most affect and transmural inflam
Smoking = RF
+ weight loss, strictures, fistulas

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31
Q

What are the features of UC?

A

CLOSEUP
Cont inflam
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis

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32
Q

When should you suspect IBD in children?

A

Perfuse diarrhoea, abdo pain, bleed, weight loss, anaemia
Systemically unwell in flares - fevers, malaise, dehydration

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33
Q

What are the extra intestinal manifestations of IBD?

A
  • Finger clubbing
  • Erythema nodosum
  • Pyoderma gangrenosum
  • Episcleritis and iritis
  • Inflam arthritis
  • Primary sclerosing cholangitis
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34
Q

What are the ix into IBD?

A
  • Bloods - FBC for anaemia, LFTs for albumin, CRP for inflam
  • Faecal calprotectin and stool sample for infective cause
  • Colonoscopy = gold standard, take biopsies to confirm diagnosis
  • CTAP if bowel obstruction or perforation for Crohn’s or toxic megacolon for UC
  • MRI can be used to assess disease severity eg. fistulae, abscesses, stricutres
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35
Q

What is the management of Crohn’s?

A

Induce remission - steroids eg. oral pred or IV hydrocortisone, immunosuppressant = azathioprine, methotrexate, adalimumab, infliximab
Maintenance - 1st line = azathioprine, alt = methotrexate, infliximab or adalimumab
Surgery - ileocaecal resection, small or large bowel resection, surgery for peri anal disease, stricturoplasty, can have anastomosis or have stoma

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36
Q

What is the management of UC?

A

Induce remission - 1st line = aminosalicylate, 2nd line = prednisolone, severe disease = IV hydrocortisone 1st line, 2nd line = IV ciclosporin
Maintenance - aminosalicylate eg. mesalazine, azathioprine
Surgery - panproctocolectomy = ileostomy or J pouch

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37
Q

What is pyloric stenosis?

A

Hypertrophy and narrowing of the pylorus, stomach = peristalsis to try and push food into duodenum, eventually food pushed into oesophagus = projective vomiting

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38
Q

What are the CF of pyloric stenosis?

A
  • Failure to thrive, thin and pale baby in first few weeks of life
  • Projectile vomiting
  • Can see peristalsis after feeding
  • Mass in upper abdomen = hypertrophic pylorus
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39
Q

What are the ABG features in pyloric stenosis?

A

Hypochloric metabolic alkalosis - vomiting HCl acid from the stomach, can also get hypokalaemia

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40
Q

What are the ix into pyloric stenosis and how is it managed?

A

IX - abdo US to see thickened pylorus
Treat - laparoscopic pyloromyotomy/Ramstedt’s operation = incision to open pylorus muscle

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41
Q

What is biliary atresia?

A

Bile duct narrowed or absent = cholestasis = conjugated bilirubin can’t be excreted

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42
Q

What is the presentation of biliary atresia?

A

Significant prolonged jaundice due to high conjugated bilirubin levels. Suspect if lasts >14 days in term babies/>21 days in premature babies.
Steatorrhoea - pale stool or yellow stool.
Jaundice can be normal in neonate but biliary atresia is serious so needs to be excluded by measuring conjugated bilirubin level.

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43
Q

What is the management of biliary atresia? What happens if you don’t treat?

A

Kasai portoenterostomy = attach section of the small intestine to the opening of the liver where the bile duct normally attaches, not always successful.
Often pt need full liver transplant for full recognition.
Untreated = cirrhosis w/i 6 months and liver failure w/i 1 year.

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44
Q

Epididymitis vs orchitis

A

Epididymitis - inflam of epididymis (sperm stored) and orchitis - inflam of testes

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45
Q

What are RF of epidiymo-orchitis?

A

Non enteric causes - MSM, multiple sexual partners, gonorrhoea
Enteric - recent instrumentation or catheterisation, bladder outlet obstruction, immunocompromised

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46
Q

What are the CF of epididymitis?

A
  • Unilat scrotal pain w swelling
  • Fevers and rigors
  • Associated sx - dysuria, storage LUTS, urethral discharge

O/e - red and swollen, tender ++, can have hydrocele, Prehn’s sign +ve

47
Q

What is Prehn’s sign?

A

Scrotal pain is relieved by elevated of tests = suggestive of epididymitis

48
Q

What are the ix into epididymitis?

A
  • Urine dip and MC+S
  • First void urine for NAAT
  • Bloods - FBC, CRP, blood cultures if systemic signs
  • US can confirm diagnosis but normally clinical is enough
49
Q

What is the management of epididymitis?

A

Abx dep on causative organism and analgesia:
Enteric - ofloxacin 200mg PO BD for 14 days
STI - ceftriaxone 500mg IM single dose and doxycycline 100mg PO BD for 10-14 days
Abstain from sexual activity until sx resolved

50
Q

What is Hirschsprung’s disease?

A

Congenital condition where parasympathetic ganglion cells of the myenteric/Auerbach’s plexus are absent in the distal bowel and rectum. Normally responsible for stim peristalsis of large bowel, no stim = food can’t pass.
Aganglionic section = constricted = bowel obstruction, proximally the bowel is distended and full.

51
Q

What is the presentation of Hirschsprung’s?

A
  • Delay in passing meconium >24 hours
  • Chronic constipation since birth
  • Abdo pain and distension
  • Vomiting
  • Poor weight gain and failure to thrive
52
Q

What is Hirschsprung associated enterocolitis? What are the CF?

A

Inflam and obstruction of the intestine occurring in 20% of those w Hirschsprung’s, 2-4 weeks of birth:
CF - fever, abdo distension, bloody diarrhoea and features of sepsis.
Is life threatening and can lead to toxic megacolon and bowel perforation.

53
Q

How do you manage HAEC?

A

IV abx, fluid resus and decompression of obstructed bowel

54
Q

What are the ix into Hirschprung’s? How is it managed?

A

Ix - AXR to diagnose, rectal biopsy
Treat - surgical removal of aganglionic section of bowel w anastomosis, risk of incontinence and leakage from anastomosis

55
Q

What are the CF of intussusception?

A
  • Severe colicky abdo pain
  • Pale lethargic unwell child
  • Redcurrant jelly stool
  • RUQ mass on palpation - sausage shaped
  • Vom
  • Bowel obstruction signs
  • Viral URTI precedes illness
56
Q

What are some conditions associated w intussusception?

A
  • Concurrent viral illness
  • Henoch Schonlein purpura
  • CF
  • Intestinal polyps
  • Meckel diverticulum
57
Q

What are the ix into intussuscpetion and how is it managed?

A

Ix - US and contrast enema
Treat - therapeutic enema = contrast, water or air pumped into colon to force bowl into normal position, if this doesn’t work will need surgical reduction, if gangrenous or perforated bowel = surgical resection

58
Q

What are the complications of intussusception and bowel obstruction?

A

Intussusception - obstruction, necrotic bowel, perforation, death
Bowel obstruction - perforation, death

59
Q

What are some causes of bowel obstruction?

A
  • Meconium ileus
  • Hirschsprung’s
  • Oesophageal or duodenal atresia
  • Intussusception
  • Imperforate anus
  • Volvulus
  • Strangulated hernia
60
Q

What are the CF of bowel obstruction?

A
  • Absolute constipation - no passing gas even
  • Abdo pain and distension
  • Faeculant/bilious vomiting
  • Abnormal bowel sounds - tinkling
61
Q

What are the ix into bowel obstruction? How is it managed?

A

Ix - AXR = dilated loops of bowel and no air in rectum, CT abdo
Manage - NBM, NG and IV - drip and suck, paeds surgical unit where will receive definitive management

62
Q

Obstruction vs ileus

A

Obstruction - mechanical cause blocking the bowel
Ileus - bowel doesn’t work properly but no structural cause

63
Q

What is volvulus? What are the CF?

A

Volvulus = twisting of a loop of bowel around its mesentary = closed loop bowel obstruction
CF - bowel obstruction signs, over a few hours, lots of abdo distension, tympanic percussion, peritonism, sepsis if perforated. Most commonly in the caecum.

64
Q

What are the ix into volvulus?

A
  • CTAP w contrast = whirl sign - corkscrew appearance of bowel
  • AXR = coffee bean
  • Bloods - U+E, Ca, TFT to exclude pseudo obstruction
65
Q

How do you manage volvulus?

A

Conservative - decompression by sigmoidoscope (relieves obstruction) and flatus tube (left in situ to cont passage of contents)
Surgical - if ischaemic or perforated or decompression failed

66
Q

What is necrotising enterocolitis?

A

One of the most common neonatal surgical emergencies. Is variable injury to the bowel = mucosal damage to necrosis and perforation, thought to be an innate immune response to the microbiota of a premature infants gut = inflam and injury.

67
Q

What are the RF of NEC?

A
  • Prematurity or v low birth weight
  • Formula feeding
  • Intrauterine growth restriction
  • Polycythaemia
  • Exchange transfusion
  • Hypoxia
  • Abnormal intestinal microbiota
68
Q

What are the CF of NEC?

A
  • Feeding intolerance
  • Vomiting - may be bile or blood stained
  • Abdo distension
  • Haematochezia - blood in stool
    + systemic features - apnoea, lethargy, brady, peripheral cyanosis
69
Q

What are the differentials for NEC?

A
  • Neonatal sepsis
  • Hirschsprung’s
  • Intestinal malrotation and volvulus
  • GORD
  • Spont perforation
  • Infectious enterocolitis
70
Q

What are the ix into NEC?

A

Plain AXR - distended bowel loops, thickened bowel wall, intramural gas, pneumoperitoneum
Bloods - FBC = anaemia, thrombocytopenia and leukopenia, U+E = hyponatraemia, ABG = metabolic acidosis, cultures

71
Q

How is NEC staged?

A

Bell scoring system:
Stage 1 - suspected NEC = bowel distension on XR, lethargy, temp instability, apnoea, brady, emesis, abdo distension, haematochezia
Stage 2 - definite NEC = bowel distension, intramural gas on XR, stage 1+ = met acidosis, thrombocytopenia, abdo tenderness, absent bowel signs
Stage 3 - adv NEC = stage 2 XR + pneumoperitoneum, stage 1+2 and severe acidosis, DIC, electrolyte imbalance, GI bleed

72
Q

What is the prophylactic management of NEC?

A

Antenatal steroids if premature delivery anticipated, breast feeding is protective

73
Q

What is the medical management of NEC?

A

Bell stage 1 and 2:
- W/hold oral feeds for 10-14 days and replace w parenteral nutrition
- IV abx for 10-14 days
- Systemic support = ventilation, fluid resus, inotropic support, correct acid base balance and coag
STAIN:
Surgical emergency
TPN - parentral nutrition
Abx
IV fluids
NBM

74
Q

What is inotropic support?

A

Stabilises circ and optimises O2 supply:
Catecholamines = noradrenaline, adrenaline, dopamine

75
Q

What is the surgical management of NEC?

A

Needed if - perforation, obstruction, deterioration despite medical management
- Intestinal resection w stoma formation most commonly
- Clip and drop procedure associated w increaed 28 day mortality

76
Q

What are the complications of NEC?

A

Perforation, sepsis, death. 50% of pt that survive develop long term complications = stricture and short bowel syndrome.
Also recurrence and neuro developmental disorders.

77
Q

What are the CF of appendicitis?

A
  • Centralised abdo pain that migrates to RIF and intensifies
  • Tenderness in McBurney’s point
  • Anorexia, N+V
  • Rovsing’s sign
  • Guarding
  • Rebound and percussion tenderness - suggest peritonitis and perforation
78
Q

What are the ix into appendicitis?

A

Normally clinical diagnosis - USS to exclude alt pathology in females. CT AP w contrast confirms diagnosis.
Diagnostic laparoscopy when clinical presentation but -ve ix.

79
Q

What is the management of appendicitis?

A

Lap appendicectomy

80
Q

What is cryptochidism?

A

Undescended tests - testes haven’t descended from the abdo, can be palpated in inguinal canal. The longer it takes for testes to descend, the less likely they will. Undescended tests = risk of testicular torsion, infertility and cancer

81
Q

What is the management of cryptochidism?

A
  • Watch and wait, most of the time will descend in 3-6 months
  • Orchidopexy if not descended in 6 months, done between 6 and 12m
82
Q

What are retractile testes?

A

Before puberty it is normal that the testes move out of the scrotum into the inguinal canal when it is cold or cremasteric reflex is activated = retractile testicles and is normal.

83
Q

What is the presentation of testicular torsion?

A
  • Sudden onset severe pain in one testicle, often following minor trauma
  • High riding teste in scrotum
  • Unilat loss of cremasteric reflex
  • -ve Prehn’s sign
  • Prepubertal or just after birth are the ages where you get it
84
Q

What is the management of testicular torsion?

A

If not treated immediately = death or damage to tissue of testicle due to ischaemia, need to remove necrotic testicle if this is the case.
Otherwise surgical exploration and fixation of the testicles w orchidoplexy - have about 6 hours to save the testis.

85
Q

What is a consequence of neonatal jaundice?

A

Kernicterus - bilirubin can cross the blood brain barrier causing permanent brain damage

86
Q

What is the differential diagnosis for neonatal jaundice?

A
  • Physiological jaundice
  • Biliary atresia
  • Haemolysis - spherocytosis, haemolytic disease of new born
87
Q

How do you manage physiological jaundice?

A
  • Establish feeds
  • Phototherapy - blue spectrum light
88
Q

What is Rigler’s sign?

A

Sign of pneumoperitoneum on AXR, can see the bowel wall on either side.

89
Q

How do you ix an undescended teste?

A

Examination under anaesthetic and diagnostic laparoscopy.
Could do USS groin and abdo but testes in an infant are tiny! Might not be able to see

90
Q

Why do you need to bring the testis down into the scrotum in undescended testes?

A
  • Prevent testicular atrophy
  • Psychologcial benefit
  • Reduce risk of trauma
  • Reduce risk of testicular cancer and can self examine
  • Optimal temp for sperm production - too hot inside body
91
Q

How do you manage hydroceoele?

A

Watch and wait - normally resolves by about 2.5 years, if hasn’t then you manage

92
Q

What is torted hydatid of morgagni?

A

Pathognonomic - blue spot sign. Has twisted on its blood supply. Just need analgesia and the bruise will go down on its own.
Hydatid of Morgagni - Mullerian remnant, has no function but can cause pain

93
Q

What is bell clapper deformity?

A
94
Q

How do you manage umbilical hernia?

A

Only operate if hernia still present by the time child starts school - is likely to close on its own. There is a low risk of strangulation or problems, is a cosmetic problem.

95
Q

Why is volvulus in a neonate so serious?

A

Most likely to affect the midgut - if it becomes ischaemic this will cause death of the bowel that is involved in absorption of nutrients - baby can’t life without it, if necrotic bowel in this section can only palliate the baby.

96
Q

What are the CF of viral hepatitis?

A

N+V, abdo pain, lethargy, jaundice - up to 50% don’t develop
Hepatomegaly, tender +/- splenomegaly
Raised LFTs but normal coag normlly

97
Q

Hep A vs Hep B vs Hep C

A

Hep A - faecal oral transmission, can be asymptomatic but most children mild illness and recover w/i 2-4w, no chronic liver disease
Hep B - perinatal transmission, infected blood via healthcare procedures, sexually. 90% of infants who get hep b perinatally = chronic carriers, older children = 5-10% carriers, 1-2% fail
Hep C - vertical transmission but can be cured

98
Q

Chronic hep b

A

30-50% of asymptomatic carrier children develop chronic disease, 10% = cirrhosis w risk hepatocellular carcinoma.
Treatment not v good

99
Q

What is acute liver failure?

A

Hepatic necrosis w loss of liver func +/- hepatic encephalopathy, uncommon but high mortality - normally caused by infection or met condition

100
Q

What are the features of acute liver failure?

A
  • Jaundice
  • Encephalopathy
  • Coagulopathy
  • Hypoglycaemia
  • Electrolyte disturb
101
Q

What are some causes of acute liver failure?

A

<2 - infection, met disease, hepatitis, drug induced
>2 - hepatitis, paracetamol overdose, Wilson’s, autoimmune hepatitis

102
Q

What is the management of acute liver failure?

A

Maintain BM >4mmol/L
Broad spectrum abx and antifungals to prevent sepsis
Prevent haemorrhage - IV vit K
Prevent cerebral oedema by fluid restriction and mannitol if oedema develops
Ultimately = liver transplant

103
Q

What are the ix into acute liver disease?

A
  • ALT and ALP elevated
  • Abnormal coag
  • Ammonia elevated
  • Need ABG
  • EEG if encephalopathy
  • CT = cerebral oedema
104
Q

What are the causes of chronic liver disease in older children?

A
  • Post viral
  • Autoimmune hepatitis and sclerosing cholangitis
  • Drug induced
  • CF - fatty liver or thick bile acid
  • Wilson’s - accumulation of copper in liver and other organs
  • Non alcoholic fatty liver disease
  • A1 antitrypsin def
105
Q

CF and ix into autoimmune hepatitis

A

CF - acute hepatitis, acute liver failure or CLD, rash, arthritis, haemoyltic anaemia
Ix - raised albumin, +ve ab
Normally - IBD, coeliac

106
Q

What is the management of autoimmune hepatitis?

A

Prednisolone and azathioprine
Sclerosing cholangitis - UDCA

107
Q

What are some complications of CLD?

A
  • Fat malabsorption = supplement fat soluble vits, steatorrhoea, protein malnutrition, anorexia
  • Pruritis in cholestasis
  • Encephalopathy
  • Cirrhosis and portal HTN, oesophageal varices, ascites, spont bacterial peritonitis
108
Q

What are the indications for liver transplant in CLD?

A
  • Severe malnutrition unresponsive to nutritional therapy
  • Complications that don’t respond to med management - bleeding varices, resistant ascites
  • Failure to grow or develop, more QOL
  • End stage liver failure
109
Q

Indirect vs direct inguinal hernia?

A

Indirect - deep inguinal ring into inguinal canal through superficial ring into groin due to incomplete closure of processus vaginalis, most common in children
Direct - through Hesselbach’s triangle, adult

110
Q

What are the ix and treatment of hernia?

A

Ix - USS, CT if obstruction or strangulation
Management - surgical repair of hernia, herniotomy on full term male infants w asymptomatic reducible inguinal hernia, emergency = irreducible

111
Q

What are the complications of hernias?

A

Recurrence
Strangulation and incarceration
Bowel obstruction

112
Q

What are the signs of peritonitis?

A

Involuntary guarding
Rebound tenderness
Fever, vom, tachy, hypotension

113
Q

What are the causes of peritonitis?

A
  • Perforation of oesophagus, ulcer, intestine eg. appendicitis
  • Infection - spont bacterial peritonitis, blood, bile or pancreatic fluid in peritoneal space
114
Q

Exompthalos vs gastroschisis?

A

Exompthalos - bowel herniates into the umbilical cord
Gastroschisis - bowel through a hole, in contact w amniotic fluid