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3a paeds > Paeds GI > Flashcards

Paeds GI Flashcards

1
Q

What is constipation

A

infrequent, difficult passage of stool that may be accompanied by the sensation of incomplete bowel emptying.

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2
Q

What are the two most common types of constipation

A

idiopathic constipation
functional constipation –> meaning there is not a significant underlying cause other than simple lifestyle factors

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3
Q

Name 3 causes of secondary causes of constipation

A
  • Hirschsprung’s disease
  • cystic fibrosis
  • hypothyroidism
  • Spinal cord lesions
  • Sexual abuse
  • Intestinal obstruction
  • Anal stenosis
  • Cows milk intolerance
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4
Q

What are typical features of constipation in history

A

Less than 3 stools a week
Hard stools that are difficult to pass
Rabbit dropping stools
Straining and painful passages of stools
Abdominal pain
Rectal bleeding associated with hard stools
Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
Loss of the sensation of the need to open the bowels

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5
Q

What are typical features of constipation in examination

A
  • Hard stools may be palpable in abdomen
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6
Q

What lifestyle factors can contribute to constipation

A
  • Habitually not opening the bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial problems such as a difficult home or school environment (always keep safeguarding in mind)
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7
Q

What are red flag signs in constipation

A
  • Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)
  • Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)
  • Vomiting (intestinal obstruction or Hirschsprung’s disease)
  • Ribbon stool (anal stenosis)
  • Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)
  • Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)
  • Failure to thrive (coeliac disease, hypothyroidism or safeguarding)
  • Acute severe abdominal pain and bloating (obstruction or intussusception)
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8
Q

What are complications of constipation

A
  • Pain
  • Reduced sensation
  • Anal fissures
  • Haemorrhoids
  • Overflow and soiling (Encopresis)
  • Psychosocial morbidity
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9
Q

How is constipation managed

A
  • Correct any reversible contributing factors, recommend a high fibre diet and good hydration
  • if impacted = polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment
  • add a stimulant laxative if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks eg lactulose

Maintenance = Movicol

  • Faecal impaction may require a disimpaction regimen with high doses of laxatives at first
  • Encourage and praise visiting the toilet. This could involve scheduling visits, a bowel diary and star charts.

Laxatives should be continued long term and slowly weaned off as the child develops a normal, regular bowel habit.

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10
Q

What is GORD

A

where contents from the stomach reflux through the lower oesophageal sphincter into the oesophagus, throat and mouth.

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11
Q

Is GORD common in babies

A

yes normal

there is immaturity of the lower oesophageal sphincter, allowing stomach contents to easily reflux into the oesophagus.

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12
Q

What % of infants stop having reflux by 1 year old

A

90%

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13
Q

What are signs of problematic reflux in babies

A

Chronic cough
Hoarse cry
Distress, crying or unsettled after feeding
Reluctance to feed
Pneumonia
Poor weight gain

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14
Q

Name some possible causes of vomiting

A

Overfeeding
Gastro-oesophageal reflux
Pyloric stenosis (projective vomiting)
Gastritis or gastroenteritis
Appendicitis
Infections such as UTI, tonsillitis or meningitis
Intestinal obstruction
Bulimia

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15
Q

What are red flag features of reflux/vomiting

A
  • Not keeping down any feed
  • Projectile or forceful vomiting
  • Bile stained vomit
  • Haematemesis or melaena
  • Abdominal distention
  • Reduced consciousness, bulging fontanelle or neurological signs
  • Respiratory symptoms (aspiration and infection)
  • Blood in the stools
  • Signs of infection
  • Rash, angioedema and other signs of allergy
  • Apnoeas
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16
Q

What is lifestyle management for reflux/vomiting

A

Small, frequent meals
Burping regularly to help milk settle
Not over-feeding
Keep the baby upright after feeding (i.e. not lying flat)

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17
Q

What treatment can be used for reflux/vomiting

A
  • Gaviscon mixed with feeds
  • Thickened milk or formula (specific anti-reflux formulas are available)
  • Proton pump inhibitors (e.g., omeprazole) where other methods are inadequate
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18
Q

What investigation can be used in severe cases of reflux/vomiting

A

barium meal and endoscopy

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19
Q

What is Sandifer’s Syndrome

A

rare condition causing brief episodes of abnormal movements cause gastro-oesophageal reflux in infants.

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20
Q

What are two ket features of Sandifer’s Syndrome

A
  • Torticollis: forceful contraction of the neck muscles causing twisting of the neck
  • Dystonia: abnormal muscle contractions causing twisting movements, arching of the back or unusual postures
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21
Q

What is Intestinal Obstruction

A

a physical obstruction prevents the flow of faeces through the intestines. This blockage will lead to a back-pressure through the gastrointestinal system, causing vomiting.

aka absolute constipation

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22
Q

what are causes Intestinal Obstruction

A

Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
Intussusception
Imperforate anus
Malrotation of the intestines with a volvulus
Strangulated hernia

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23
Q

How does Intestinal Obstruction present

A
  • Persistent vomiting. This may be bilious, containing bright green bile.
  • Abdominal pain and distention
  • Failure to pass stools or wind
  • Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later.
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24
Q

what is the initial investigation of choice for Intestinal Obstruction

A

abdominal xray.

  • dilated loops of bowel proximal to the obstruction
  • absence of air in the rectum.
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25
Q

What is initial management for Intestinal Obstruction

A
  • nil by mouth & inserting a NG tube to help drain the stomach and stop the vomiting.
  • IV fluids to correct any dehydration and electrolyte imbalances, and keep them hydrated while waiting for definitive management of the underlying cause.
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26
Q

What is Pyloric Stenosis

A

Hypertrophy (thickening) and therefore narrowing of the pylorus

prevents food traveling from the stomach to the duodenum as normal.

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27
Q

what is a pyloric sphincter

A

a ring of smooth muscle the forms the canal between the stomach and the duodenum

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28
Q

How does pyloric stenosis present

A

presents in the first few weeks of life, with a hungry baby that is thin, pale and generally failing to thrive

** “projectile vomiting” **

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29
Q

how does pyloric stenosis present after feeding

A

peristalsis can be seen by observing the abdomen
firm, round mass can be felt in the upper abdomen –> hypertrophic muscle of pylorus

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30
Q

what does pyloric stenosis show on blood gas analysis

A

hypochloric (low chloride) metabolic alkalosis as the baby is vomiting the hydrochloric acid

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31
Q

How is pyloric stenosis diagnosed

A

abdominal ultrasound to visualise the thickened pylorus

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32
Q

How is pyloric stenosis treated

A

laparoscopic pyloromyotomy (known as “Ramstedt’s operation“)

An incision is made in the smooth muscle of the pylorus to widen the canal allowing that food to pass from the stomach to the duodenum as normal.

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33
Q

how does pyloric stenosis present on blood gas

A

hypochloraemic hypokalaemic alkalosis

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34
Q

What is the prognosis following laparoscopic pyloromyotomy

A

excellent

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35
Q

What is Gastroenteritis

A

inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

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36
Q

What is Acute gastritis

A

inflammation of the stomach and presents with nausea and vomiting.

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37
Q

what is Enteritis

A

inflammation of the intestines and presents with diarrhoea

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38
Q

What is the MC cause of Gastroenteritis

A

viral causes - rotavirus in children

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39
Q

What is the main concern in Gastroenteritis

A

dehydration

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40
Q

What are DDx of Diarrhoea

A
  • Infection (gastroenteritis)
  • Inflammatory bowel disease
  • Lactose intolerance
  • Coeliac disease
  • Cystic fibrosis
  • Toddler’s diarrhoea
  • Irritable bowel syndrome
  • Medications (e.g. antibiotics)
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41
Q

What is the key management establishment needed for Gastroenteritis

A

whether they are able to keep themselves hydrated or whether they need admission for IV fluids

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42
Q

What are 2 common viral causative agents of gastroenteritis

A

Rotavirus
Norovirus

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43
Q

What e coli strain produced shiga toxin

A

E. coli 0157

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44
Q

how is e. coli spread

A

infected faeces, unwashed salads or contaminated water

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45
Q

What are symptoms of shiga toxin

A

abdominal cramps, bloody diarrhoea and vomiting

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46
Q

what can shiga toxin lead to

A

destroys blood cells and leads to haemolytic uraemic syndrome (HUS).

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47
Q

is the use of Abx indicated in shiga toxin

A

No, bc the use of antibiotics increases the risk of haemolytic uraemic syndrome

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48
Q

What is the MC bacterial cause of gastroenteritis worldwide

A

Campylobacter - “travellers diarrhoea”

gram negative bacteria that has a curved or spiral shap

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49
Q

How is Campylobacter spread

A

Raw or improperly cooked poultry
Untreated water
Unpasteurised milk

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50
Q

What are symptoms of Campylobacter Jejuni

A

flu-like prodrome peroid then
Abdominal cramps
Diarrhoea often with blood
Vomiting
Fever

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51
Q

is the use of Abx indicated in Campylobacter Jejuni

A

yes after ID organism with severe symptoms or RF like <3 failure or HIV

–> azithromycin or ciprofloxacin.

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52
Q

What is incubation and resolution period for Campylobacter

A

Incubation is usually 2 to 5 days. Symptoms resolve after 3 to 6 days

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53
Q

What is incubation and resolution period for shigella

A

incubation period is 1 to 2 days and symptoms usually resolve within 1 week without treatment

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54
Q

what is Bacillus Cereus

A

gram positive rod spread through inadequately cooked food.

fried rice

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55
Q

What toxin does Bacillus Cereus produce

A

cereulide

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56
Q

how does Bacillus Cereus present

A
  • causes abdominal cramping and vomiting within 6 hours of ingestion
  • watery diarrhoea after 6 hours
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57
Q

how long does it take for Bacillus Cereus to resolve

A

24 hours

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58
Q

What is Giardiasis

A

Giardia lamblia is a type of microscopic parasite. It lives in the small intestines of mammals.

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59
Q

What is the transmission pathway of giardiasis

A

faecal-oral transmission.

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60
Q

How is Giardiasis diagnosed

A

stool microscopy

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61
Q

How is Giardiasis treated

A

metronidazole

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62
Q

What can prevent gastroenteritis

A

Good hygiene

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63
Q

what is important hospital/home management for preventing spread of gastroenteritis

A
  • Barrier nursing
  • rigorous infection control
  • Children need to stay off school until 48 hours after the symptoms have completely resolved.
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64
Q

how is causative organism and antibiotic sensitivities established in gastroenteritis

A

microscopy, culture and sensitivities stool sample

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65
Q

How are patients determines to tolerate self hydration and not require hospital admission for gastroenteritis

A

fluid challenge.

involves recording a small volume of fluid given orally every 5-10 minutes to ensure they can tolerate it.

If they are able to tolerate oral fluid and are adequately hydrated they can usually be managed at home

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66
Q

Name a Rehydration solution

A

dioralyte

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67
Q

name an antidiarrhoeal medication

A

loperamide

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68
Q

name an antiemetic medication

A

metoclopramide

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69
Q

Are Antidiarrhoeal and antiemetic medications recommended gastroenteritis

A

no

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70
Q

Name post-gastroenteritis complications

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

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71
Q

What are primary features of Crohns

A

N – No blood or mucus (these are less common in Crohns.)
E – Entire GI tract
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor (don’t set the nest on fire)

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72
Q

What are primary features of Ulcerative Colitis

A

C – Continuous inflammation
L – Limited to colon and rectum
O – Only superficial mucosa affected
S – Smoking is protective
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary sclerosing cholangitis

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73
Q

What are IBD

A

Crohns
Ulcerative Colitis

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74
Q

How does IBD present

A

perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia.

systemically unwell during flares, with fevers, malaise and dehydration.

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75
Q

What are extra-intestinal manifestations of IBD

A

Finger clubbing
Erythema nodosum
Pyoderma gangrenosum
Episcleritis and iritis
Inflammatory arthritis
Primary sclerosing cholangitis (ulcerative colitis)

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76
Q

What blood tests can be ordered to investiagte IBD

A
  • Full blood count for haemoglobin (low in anaemia) and platelet count (raised with inflammation)
  • C-reactive protein (CRP) -> inflammation
  • Urea and electrolytes (U&Es) indicate electrolyte imbalances and kidney function
  • Liver function tests (LFTs) can show low albumin in severe disease (protein is lost in the bowel)
  • Thyroid function tests for hyperthyroidism as a cause of diarrhoea
  • Anti-tissue transglutaminase antibodies (anti-TTG) for coeliac disease as a differential diagnosis
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77
Q

What initial investigation is ordered for IBD

A

Faecal calprotectin

90% sensitive and specific for inflammatory bowel disease

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78
Q

What is the gold standard investigation for diagnosis of IBD

A

Endoscopy (Oesophago-gastroduodenoscopy and colonoscopy) with biposy

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79
Q

What imagining investigations can be ordered to look for complications of IBD

A

ultrasound, CT and MR

eg fistulas, abscesses and strictures

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80
Q

What MDT members might be involved in IBD care

A

paediatricians, specialist nurses, pharmacists, dieticians and surgeons

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81
Q

What is essential to monitor in children with IBD

A

monitor the growth and pubertal development

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82
Q

How are acute flares of crohns managed

A

First line are steroids (e.g. oral prednisolone or IV hydrocortisone).

if doesnt work consider + immunosuppressant medication

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83
Q

How is remission maintained in crohns

A

1st line
- Azathioprine
- Mercaptopurine

alt

-Methotrexate
- Infliximab
- Adalimumab

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84
Q

What is surgical management of crohns

A

surgically resect distal ileum

treat strictures and fistulas secondary to Crohn’s

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85
Q

How are acute flares of UC in mild to moderate disease maanged

A

1st line –> aminosalicylate (e.g. mesalazine oral or rectal)

2nd line –> corticosteroids (e.g. prednisolone)

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86
Q

How are acute flares managed in UC in severe disease

A

1st line –> IV corticosteroids (e.g. hydrocortisone)

2nd line –> IV ciclosporin

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87
Q

How is maintaining remission managed in UC

A
  • Aminosalicylate (e.g. mesalazine oral or rectal)
  • Azathioprine
  • Mercaptopurine
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88
Q

What is surgical management of UC

A

Ulcerative colitis usually only affects the colon and rectum –>

removing the colon and rectum (panproctocolectomy)

permanent ileostomy

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89
Q

What is IBS

A

disturbance of the gut-brain interaction, resulting in troublesome abdominal and intestinal symptoms

functional disorder –> no ID bowel disease, abnormal function with normal bowel

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90
Q

What are 3 keys symptoms of IBS

A

I – Intestinal discomfort (abdominal pain relieved by opening bowels)
B – Bowel habit abnormalities (frequency)
S – Stool abnormalities (watery, loose, hard or associated with mucus)

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91
Q

what are common symptoms of IBS

A

Abdominal pain
Diarrhoea
Constipation
Fluctuating bowel habit
Bloating
Worse after eating
Improved by opening bowels
Passing mucus

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92
Q

What can trigger or worsen IBS symptoms

A

Anxiety
Depression
Stress
Sleep disturbance
Illness
Medications
Certain foods
Caffeine
Alcohol

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93
Q

What are DDx of IBS

A
  • Bowel cancer
  • Inflammatory bowel disease
  • Coeliac disease
  • Ovarian cancer (often presents with vague symptoms, particularly bloating in women over 50 years)
  • Pancreatic cancer
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94
Q

How blood tests can be order to investigate DDx for IBS

A
  • Full blood count for anaemia
  • Inflammatory markers (e.g., ESR and CRP)
  • Coeliac serology (e.g., anti-TTG antibodies)
  • Faecal calprotectin for inflammatory bowel disease
  • CA125 for ovarian cancer
95
Q

How is IBS diagnosed

A

diagnosis of exclusion

at least 6 months of abdominal pain or discomfort with at least one of:
- Pain or discomfort relieved by opening the bowels
- Bowel habit abnormalities (more or less frequent)
- Stool abnormalities (e.g., watery, loose or hard)

also require at least two of:
- Straining, an urgent need to open bowels or incomplete emptying
- Bloating
- Worse after eating
- Passing mucus

96
Q

What lifestyle advice can be given for IBS

A
  • Drinking enough fluids
  • Regular small meals
  • Adjusting fibre intake according to symptoms
  • Limit caffeine, alcohol and fatty foods
  • Low FODMAP diet, guided by a dietician
  • Probiotic supplements may be considered over-the-counter
  • Reduce stress where possible
  • Regular exercise
97
Q

What is a medication for diarrhoea

A

Loperamide

98
Q

what is a medication for constipation

A

ispaghula husk

99
Q

what medication can be used for abdominal cramps

A

Antispasmodics

mebeverine, alverine, hyoscine butylbromide or peppermint oil

however weak evidence

100
Q

What medication can be used for constipation in IBS when first-line laxatives are inadequate.

A

Linaclotide

101
Q

What are other management options when IBS symptoms remain uncontrolled (psych adjacent)

A
  • Low-dose tricyclic antidepressants (e.g., amitriptyline)
  • SSRI antidepressants
  • Cognitive behavioural therapy (CBT)
  • Specialist referral for further management
102
Q

what is Hirschsprung’s

A

congenital condition where nerve cells of the myenteric plexus are absent in the distal bowel and rectum

absence of parasympathetic ganglion cells

103
Q

what is myenteric plexus also known as and what does it form

A

Auerbach’s plexus

forms the enteric nervous system. It is the brain of the gut.

104
Q

What does myenteric plexus do

A

responsible for stimulating peristalsis of the large bowel.

GI tract motility

105
Q

What is the pathophysiology of development of Hirschsprung’s

A

when the parasympathetic ganglion cells do not travel all the way down the colon in fetal development, and a section of colon at the end is left without these parasympathetic ganglion cells.

106
Q

What is it called when the entire colon is affected by Hirschsprung’s

A

total colonic aganglionosis

107
Q

Is the part of the colon affected by Hirschsprung’s constricted or relaxed

A

The aganglionic section of colon does not relax, causing it to becomes CONSTRICTED

108
Q

What conditions are associated with Hirschsprung’s

A
  • Downs syndrome
  • Neurofibromatosis
  • Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)
  • Multiple endocrine neoplasia type II
109
Q

How does Hirschsprung’s present

A
  • presents in neonate peroid
  • Delay in passing meconium (more than 24 hours)
  • Chronic constipation since birth
  • Abdominal pain and distention
  • Vomiting
  • Poor weight gain and failure to thrive
  • After the PR there may be an improvement in symptoms
110
Q

What is Hirschsprung-Associated Enterocolitis

A

inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease.

111
Q

What is a life threatening complication of Hirschsprung in neonates

A

Hirschsprung-associated enterocolitis

can lead to toxic megacolon and perforation of the bowel.

112
Q

How does Hirschsprung-associated enterocolitis present

A

within 2-4 weeks of birth

with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis.

113
Q

how is Hirschsprung-associated enterocolitis managed

A

urgent IV antibiotics, fluid resuscitation and decompression of the obstructed bowel.

114
Q

What is 1st line investigation for Hirschsprung

A

Abdominal xray can be helpful in diagnosing intestinal obstruction

115
Q

How is Hirschsprung diagnosis confirmed and what will it show

A

Rectal biopsy

histology will show absence of ganglionic cells.

116
Q

What is the definitive management of Hirschsprung

A

surgical removal of the aganglionic section of bowel

117
Q

What is coeliac disease

A

autoimmune condition where exposure to gluten causes an immune reaction that creates inflammation in the small intestine

118
Q

what autoantibodies do people with coeliac disease produce in response to gluten exposure

A
  • anti-tissue transglutaminase (anti-TTG)
  • anti-endomysial (anti-EMA).
119
Q

What cells are targeted in coeliac disease

A

epithelial cells

120
Q

Where does inflammation in coeliac disease affect

A

small bowel, particularly the jejunum.

121
Q

How does coeliac disease cause malabsorption

A

causes atrophy of the intestinal villi

122
Q

What human leukocyte antigen (HLA) are associated with coeliac disease

A

HLA-DQ2
HLA-DQ8

123
Q

A new diagnosis of what two conditions requires testing for coeliac disease

A

type 1 diabetes & autoimmune thyroid disease

124
Q

How does Coeliac disease present

A

often asymptomatic

  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia secondary to iron, B12 or folate deficiency
  • Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen
125
Q

What are rare neurological symptoms of Coeliac disease

A

Peripheral neuropathy
Cerebellar ataxia
Epilepsy

126
Q

What class of antibody is Anti-TTG and anti-EMA antibodies

A

IgA

127
Q

What is important to remember when testing for antibodies in coeliac

A

to test for total Immunoglobulin A levels

–> if total IgA is low the coeliac test will be negative even when they have the condition

128
Q

What are first line blood tests for coeliac

A
  • Raised anti-TTG antibodies (first choice)
  • Raised anti-endomysial antibodies
  • Total immunoglobulin A levels to exclude IgA deficiency
129
Q

what is the definitive diagnosis for coeliac and what are the findings

A

Endoscopy and intestinal biopsy

  • Crypt hyperplasia
  • Villous atrophy
130
Q

How is coeliac managed

A

lifelong gluten-free diet

131
Q

what are complications of untreated coeliac

A
  • Nutritional deficiencies
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL)
  • Non-Hodgkin lymphoma
  • Small bowel adenocarcinoma
132
Q

What is Appendicitis

A

inflammation of the appendix

133
Q

What part of the bowel is the appendix attached to

A

caecum

134
Q

What causes appendicitis

A

becomes inflamed due to infection trapped in the appendix by obstruction at the point where the appendix meets the bowel

135
Q

What can untreated appendicitis lead to

A

gangrene and rupture
peritonitis

136
Q

What is the peak incidence of appendicitis

A

10 to 20 years.

137
Q

What is the central presenting feature of appendicitis

A

central abdominal pain, that moves down to the right iliac fossa (RIF) over time and eventually becomes localised in the RIF

138
Q

What is the examination finding for appendicitis

A

Tenderness in McBurney’s point.
Rovsing’s sign
Rebound tenderness
Guarding on abdo palpation
Percussion tenderness

139
Q

Where is McBurney’s point

A

one third the distance from the anterior superior iliac spine (ASIS) to the umbilicus.

140
Q

What is Rovsings sign

A

palpation of the left iliac fossa causes pain in the RIF

141
Q

What is rebound tenderness

A

increased pain when quickly releasing pressure on the right iliac fossa

142
Q

What does rebound tenderness and percussion tenderness suggest

A

peritonitis, caused by a ruptured appendix.

143
Q

How is appendicitis diagnosed

A

clinical presentation and raised inflammatory markers

CT Scan/US to excluded obgyn ddx

144
Q

What is the investigation when a patient has a clinical presentation suggestive of appendicitis but investigations are negative

A

perform a diagnostic laparoscopy to visualise the appendix directly.

145
Q

What are key DDx of appendicitis

A
  • Ectopic Pregnancy
  • Ovarian Cysts
  • Meckel’s Diverticulum
  • Mesenteric Adenitis
  • Appendix mass
146
Q

How is appendicitis managed

A

emergency admission to hospital under the surgical team

definitive = Removal of the inflamed appendix (appendicectomy) Laparoscopic

147
Q

What are Complications of Appendicectomy

A
  • Bleeding, infection, pain and scars
  • Damage to bowel, bladder or other organs
  • Removal of a normal appendix
  • Anaesthetic risks
  • Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
148
Q

What is intussusception

A

condition where the bowel “invaginates” or “telescopes” into itself.

This thickens the overall size of the bowel and narrows the lumen at the folded area, leading to a palpable mass in the abdomen and obstruction to the passage of faeces through the bowel. I

149
Q

Who does Intussusception typically affect

A

infants 6 months to 2 years
more common in boys.

150
Q

What conditions is intussusception associated with

A
  • Concurrent viral illness
  • Henoch-Schonlein purpura
  • Cystic fibrosis
  • Intestinal polyps
  • Meckel diverticulum
151
Q

How does intussusception present

A
  • ** redcurrant jelly stool **
  • ** Right upper quadrant mass on palpation. This is described as “sausage-shaped” **
  • Severe, colicky abdominal pain
  • Pale, lethargic and unwell child
  • viral URT infection
  • Vomiting
  • Intestinal obstruction
152
Q

How is intussusception diagnosed

A

ultrasound scan
A classic target or bull’s eye sign seeen

153
Q

What is first line management for intussusception

A

Therapeutic enemas - reduction with air insufflation

Contrast, water or air are pumped into the colon to force the folded bowel out of the bowel and into the normal position.

154
Q

What is the management when enemas do not work

A

Surgical reduction

155
Q

When is surgical resection required for intussusception

A

If the bowel becomes gangrenous (due to a disruption of the blood supply) or the bowel is perforated

156
Q

what are complications of intussusception

A

Obstruction
Gangrenous bowel
Perforation
Death

157
Q

What is biliary atresia

A

congenital condition where a section of the bile duct is either narrowed or absent.

158
Q

What does biliary atresia result in

A

results in cholestasis

bile cannot be transported from the liver to the bowel

= prevents the excretion of conjugated bilirubin

159
Q

When should biliary atresia be suspected

A

in babies with a persistent jaundice, lasting more than 14 days in term babies and 21 days in premature babies

160
Q

What is initial investigation for biliary atresia

A

conjugated and unconjugated bilirubin

will have high conjugated bilirubin levels

161
Q

Why is conjugated bilirubin high in biliary atresia

A

the liver is processing the bilirubin for excretion (by conjugating it), but it is not able to excrete the conjugated bilirubin because it cannot flow through the biliary duct into the bowel.

162
Q

How is biliary atresia managed

A

surgical

“Kasai portoenterostomy”

creating a connection between the liver and the small intestine to allow for bile drainage

163
Q

What is a hernia

A

weakness in cavity wall that allows body organ (e.g., bowel) that would normally be contained within that cavity to pass through the cavity wall

164
Q

how does a hernia present

A
  • A soft lump protruding from the abdominal wall
  • The lump may be reducible (it can be pushed back into the normal place)
  • The lump may protrude on coughing (raising intra-abdominal pressure) or standing (pulled out by gravity)
  • Aching, pulling or dragging sensation
165
Q

What are three key complications of hernias

A
  • Incarceration
  • Obstruction
  • Strangulation
166
Q

what is hernia incarceration

A

where the hernia cannot be reduced back into the proper position

167
Q

what is hernia obstruction

A

where a hernia causes a blockage in the passage of faeces through the bowel.

168
Q

what is hernia strangulation

A

where a hernia is non-reducible (it is trapped with the bowel protruding) and the base of the hernia becomes so tight that it cuts off the blood supply, causing ischaemia.

169
Q

What feature of hernias is used to formulate risk assessment and management plan

A

size of the neck/defect (narrow or wide)

Hernias that have a wide neck, meaning that the size of the opening that allows abdominal contents through is large, are at lower risk of complications.

170
Q

What are the 3 general principles of hernia management

A

Conservative management
Tension-free repair (surgery)
Tension repair (surgery)

171
Q

What is conservative management for abdominal hernias

A

involves leaving the hernia alone

most appropriate when the hernia has a wide neck

172
Q

What is tension free repair for abdominal hernias

A

placing a mesh over the defect in the abdominal wall.
Mesh is sutured to the muscles and tissues on either side of the defect, covering it and preventing herniation of the cavity contents.

MC

173
Q

what is a tension repair of abdominal hernias

A

suture the muscles and tissue on either side of the defect back together

174
Q

What are two types of inguinal hernias

A

Indirect inguinal hernia
Direct inguinal hernia

175
Q

What is a Direct inguinal hernia

A

hernia protrudes directly through the abdominal wall, through Hesselbach’s triangle

176
Q

What is an indirect inguinal hernia

A

the bowel herniates through the inguinal canal.

goes into scrotum

177
Q

What are DDx for inguinal hernia

A
  • Femoral hernia
  • Lymph node
  • Saphena varix (dilation of saphenous vein at junction with femoral vein in groin)
  • Femoral aneurysm
  • Abscess
  • Undescended / ectopic testes
  • Kidney transplant
178
Q

How do you differentiate direct from indirect inguinal hernias

A

in INDIRECT hernias –> when pressure is applied to the deep inguinal ring, the hernia will remain reduced.

pressure over deep inguinal ring will not stop herniation in direct

179
Q

when is the deep inguinal ring located

A

at the mid-way point from the ASIS to the pubic tubercle

180
Q

What are boundaries of Hesselbach’s triangle

A
  • R – Rectus abdominis muscle – medial border
  • I – Inferior epigastric vessels – superior / lateral border
  • P – Poupart’s ligament (inguinal ligament) – inferior border
181
Q

What is Cow’s Milk Protein Allergy

A

hypersensitivity to the protein in cow’s milk

typically affecting infants and young children under 3 years.

182
Q

how can Cow’s Milk Protein Allergy reaction occur

A

IgE mediated –> rapid reaction w/in 2 hours

non-IgE medicated –> occurring slowly over several days

183
Q

Who is cow’s milk protein allergy more common in

A

more common in formula fed babies and those with a personal or family history of other atopic conditions.

184
Q

What are gastrointestinal symptoms of cow’s milk protein allergy

A
  • Bloating and wind
  • Abdominal pain
  • Diarrhoea
  • Vomiting
185
Q

what are general allergic symptoms of cow’s milk protein allergy

A
  • Urticarial rash (hives)
  • Angio-oedema (facial swelling)
  • Cough or wheeze
  • Sneezing
  • Watery eyes
  • Eczema
186
Q

How is cow’s milk protein allergy diagnosed

A

based on a full history and examination

Skin prick testing can help support the diagnosis but is not always necessary

187
Q

How is cow’s milk protein allergy managed

A

Avoiding cow’s milk should fully resolve symptoms:

Breast feeding mothers should avoid dairy products
Replace formula with special hydrolysed formulas designed for cow’s milk allergy –> protein removed

188
Q

What is prognosis for cow’s milk protein allergy

A

Most children will outgrow cow’s milk protein allergy by age 3, often earlier

189
Q

What steps should be taken to resolve cow’s milk protein allergy

A

Every 6 months or so, infants can be tried on the first step of the milk ladder and then slowly progress up the ladder until they develop symptoms

190
Q

What is Meckel’s diverticulum

A
  • congenital diverticulum of the small intestine
  • remnant of the omphalomesenteric duct
  • occurs in 2% of the population
  • is 2 feet from the ileocaecal valve
  • is 2 inches long
191
Q

How is Meckel’s diverticulum investigated

A

FBC
technetium-99m pertechnetate scan (‘Meckel’s scan’)

192
Q

How does Meckel’s diverticulum present

A

usually asymptomatic

however it can bleed, become inflamed, rupture or cause a volvulus or intussusception

passage of bright red stool
intractable constipation

number 1 cause of painless massive GI bleeding in 1-2yr

193
Q

How is Meckel’s diverticulum managed

A

if asymptomatic –> treatment not required

if symptomatic –> excision of diverticulum

194
Q

What is Kwashiorkor

A

dietary protein deficiency

195
Q

What is Kwashiorkor associated with

A

corn-based diet, recent weaning, measles, or diarrhoeal illness

196
Q

How does Kwashiorkor present

A

affects children 6months to 3 years
bilateral pitting oedema, in the absence of another medical cause of oedema
protruding stomach

197
Q

What is Failure to thrive

A

poor physical growth and development in a child

198
Q

what is Faltering growth

A

as a fall in weight across:

  • One or more centile spaces if their birthweight was below the 9th centile
  • Two or more centile spaces if their birthweight was between the 9th and 91st centile
  • Three or more centile spaces if their birthweight was above the 91st centile
199
Q

What are causes of Failure to Thrive

A

Inadequate nutritional intake
Difficulty feeding
Malabsorption
Increased energy requirements
Inability to process nutrition

200
Q

what are causes of inadequate nutritional intake

A

Maternal malabsorption if breastfeeding
Iron deficiency anaemia
Family or parental problems
Neglect
Availability of food (i.e. poverty)

201
Q

what are causes of difficulty feeding

A

Poor suck, for example due to cerebral palsy
Cleft lip or palate
Genetic conditions with an abnormal facial structure
Pyloric stenosis

202
Q

What are causes of malabsorption

A

Cystic fibrosis
Coeliac disease
Cows milk intolerance
Chronic diarrhoea
Inflammatory bowel disease

203
Q

what are causes of increaaed energy requirements

A

Hyperthyroidism
Chronic disease, for example congenital heart disease and cystic fibrosis
Malignancy
Chronic infections, for example HIV or immunodeficiency

204
Q

what are causes of inability to process nutrients properly

A

Inborn errors of metabolism
Type 1 diabetes

205
Q

what is the aim of assessment for failure to thrive

A

establish the cause of the failure to thrive

206
Q

What key areas need to be assessed in a failure to thrive assessment

A
  • Height, weight and BMI (if older than 2 years) and plotting these on a growth chart **
  • Calculate the mid-parental height centile **
  • Pregnancy, birth, developmental and social history
  • Feeding or eating history
  • Observe feeding
  • Mums physical and mental health
  • Parent-child interactions
207
Q

what does a feeding history involve

A

breast or bottle feeding
feeding times
volume
frequency
any difficulties with feeding

208
Q

what does an eating history involve

A

food choices
food aversion
meal time routines
appetite in children

209
Q

how is BMI calculated

A

(weight in kg) / (height in meters)2.

210
Q

how is mid parental height calculated

A

(height of mum + height of dad) / 2.

211
Q

What outcome of BMI or mid parental height centile suggests an inadequate nutrition or a growth disorder are:

A
  • Height more than 2 centile spaces below the mid-parental height centile
  • BMI below the 2nd centile
212
Q

What are initial investigations for failure to thrive

A

Urine dipstick, for urinary tract infection
Coeliac screen (anti-TTG or anti-EMA antibodies)

213
Q

What support is there for difficulty breast feeding

A

midwives, health visitors, peers groups and “lactation consultants”.

Supplementing with formula milk

214
Q

what are management options when inadequate nutrition is cause of faltering growth

A
  • Encouraging regular structured mealtimes and snacks
  • Reduce milk consumption to improve appetite for other foods
  • Review by a dietician
  • Additional energy dense foods to boost calories
  • Nutritional supplements drinks
215
Q

what is marasmus

A

due to deficiency of proteins and calories

216
Q

how does marasmus present

A

severe reduction in body weight
shrunken abdo
prominent ribs
no fatty liver and no oedema

217
Q

What is a choledochal cyst

A

rare, congenital condition that causes the bile ducts to swell before birth

218
Q

how does a choledochal cyst present

A

Abdominal pain, palpable abdominal mass, and jaundice

219
Q

How are choledochal cyst investigated

A

US
CT cholangiography - more accurate
Technectium-99 HIDA scan

220
Q

what is the gold standard investigation for choledochal cyst

A

Magnetic Resonance Cholangiopancreatography (MRCP)

221
Q

How is choledochal cyst managed

A

radical surgical excision

222
Q

What are complications of choledochal cyst

A

Malignancy
Stricture
Ascending Cholangitis
Sludge and Stone Formation

223
Q

What are DDx for choledochal cyst

A

Hepatic cysts
Duodenal atresia
Mesenteric or omental cysts
Intestinal duplication
Gallbladder duplication
Ovarian cysts

224
Q

What is neonatal hepatitis

A

inflammation of the liver that occurs only in early infancy, usually between one and two months after birth

225
Q

Name infective causes of neonatal hepatitis

A

cytomegalovirus, rubella (measles) and hepatitis A, B or C viruses.

226
Q

How is neonatal hepatitis investigated

A

liver biopsy
blood tests

227
Q

How does neonatal hepatitis present

A

jaundice
enlarged liver

228
Q

how is neonatal hepatitis differentied from biliary atresia

A

liver biopsy

often show that four or five liver cells are combined into a large cell w poor function

229
Q

How is neonatal hepatitis treated

A

no specific treatment for neonatal hepatitis

230
Q

what is phenobarbital

A

stimulates the liver to excrete additional bile

231
Q

what is key sign of intestinal malrotation

A

bilious vomiting

he green colour of the vomit is caused by conditions that cause intestinal obstruction distal to the ampulla of Vater. After this point, the bile is mixed with the intestinal contents, giving the vomit the classical green colour

232
Q

what is intestinal malrotation associated with

A

Exomphalos and diaphragmatic herniae

233
Q

how is intestinal malrotation with volvulus managed

A

Ladd’s procedure

3a paeds (12 decks)

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