Paeds gastro Flashcards

1
Q

Presentation of appendicitis in children?

A

This typically starts as central abdominal pain, that moves down to the right iliac fossa (RIF) over time and eventually becomes localised in the RIF. On palpation of the abdomen there is tenderness in McBurney’s point.

Loss of appetite (anorexia)
Nausea and vomiting
Rovsing’s sign (palpation of the left iliac fossa causes pain in the RIF)
Guarding on abdominal palpation
Rebound tenderness is increased pain when quickly releasing pressure on the right iliac fossa
Percussion tenderness is pain and tenderness when percussing the abdomen
Rebound tenderness and percussion tenderness suggest peritonitis, caused by a ruptured appendix.

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2
Q

What are some differentials you might consider when thinking about appendicitis?

A

*Ectopic!!!!!!!!!!!!!!!!!!!!!!!
*Ovarian cysts
*Meckels diverticulum
*Appendix mass

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3
Q

Investigating appendicitis

A

clinical presentation and raised inflammatory markers. Performing a CT scan can be useful in confirming the diagnosis, particularly where another diagnosis is more likely. An ultrasound scan is often used in female patients to exclude ovarian and gynaecological pathology.

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4
Q

Intussusception wtf is it?

A

Intussusception is a condition where the bowel “invaginates” or “telescopes” into itself. Picture the bowel folding inwards. 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. It typically occurs in infants 6 months to 2 years and is more common in boys.

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5
Q

Presentation of intussusception

A

REDCURRANT JELLY STOOL!!!!
RUQ MASS - SAUSAGE SHAPED ON PALPATION
he typical child in the exam will have had a viral upper respiratory tract infection preceding the illness and will have features of intestinal obstruction (vomiting, absolute constipation and abdominal distention). Ultrasound is the initial investigation of choice.

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6
Q

Mx of intussusception

A

iagnosis is made mainly by ultrasound scan or contrast enema.

Therapeutic enemas can be used to try to reduce the intussusception
If the bowel becomes gangrenous (due to a disruption of the blood supply) or the bowel is perforated, then surgical resection is required.

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7
Q

Causes of 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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8
Q

Whats the px of intestinal obstruction?

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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9
Q

how would you ix intestinal obstruction

A

abdominal xray. This may show dilated loops of bowel proximal to the obstruction and collapsed loops of bowel distal to the obstruction. There will also be absence of air in the rectum

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10
Q

How would you mx an intestinal obstruction?

A

paediatric surgical unit as an emergency. Initial management involves making them nil by mouth and inserting a nasogastric tube to help drain the stomach and stop the vomiting. They will also require 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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11
Q

What is biliary atresia ? How does it present ?

A

a section of the bile duct is either narrowed or absent. This results in cholestasis, where the bile cannot be transported from the liver to the bowel. Conjugated bilirubin is excreted in the bile, therefore biliary atresia prevents the excretion of conjugated bilirubin.
Px: Jaundice

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12
Q

Mx of biliary atresia?

A

Management of biliary atresia is with surgery. The “Kasai portoenterostomy” involves attaching a section of the small intestine to the opening of the liver, where the bile duct normally attaches. This is somewhat successful and can clear the jaundice and prolong survival. Often patients require a full liver transplant to resolve the condition

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13
Q

Features of Crohns

A

Crohn’s (crows NESTS)

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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14
Q

Features of UC

A

Ulcerative Colitis (remember U – C – CLOSEUP)

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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15
Q

Px of IBD in children?

A

Suspect inflammatory bowel disease in children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration.

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

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16
Q

Testing for IBD?

A

Faecal calprotectin is released by the intestines when inflamed. It is a useful screening test and is more than 90% sensitive and specific for IBD in adults.

Endoscopy (OGD and colonoscopy) with biopsy is the gold standard investigation for diagnosis of IBD.

Imaging with ultrasound, CT and MRI can be used to look for complications such as fistulas, abscesses and strictures.
Raised CRP in bloods -> Active inflammation

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17
Q

Mx of Crohns

A

1st line : Steroids - PO prednisolone or IV hydrocortisone
Azathioprine after to maintain remission - immunosup

18
Q

Management of UC

A

Mild to moderate disease

First line: aminosalicylate (e.g. mesalazine oral or rectal)
Second line: corticosteroids (e.g. prednisolone)
Severe disease

First line: IV corticosteroids (e.g. hydrocortisone)
Second line: IV ciclosporin

Azathioprine or mesalazine for remission

19
Q

Surgical option for UC?

A

Ulcerative colitis usually only affects the colon and rectum. Therefore, removing the colon and rectum (panproctocolectomy) will remove the disease. The patient is then left with either a permanent ileostomy or something called an ileo-anal anastomosis (J-pouch). This is where the ileum is folded back on itself and fashioned into a larger pouch that functions like a rectum. This “J-pouch” is then attached to the anus and collects stools prior to the person passing a motion.

20
Q

Psthophysio of coeliac disease

A

In coeliac disease autoantibodies are created in response to exposure to gluten. These autoantibodies target the epithelial cells of the intestine and lead to inflammation. There are two antibodies to remember: anti-tissue transglutaminase (anti-TTG) and anti-endomysial (anti-EMA).

21
Q

Px of coeliac

A

Coeliac disease is often asymptomatic, so have a low threshold for testing for coeliac disease in patients where it is suspected. Symptoms can include:

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

22
Q

What are you looking for in coeliac tests?

A

Anti-TTG and anti-EMA antibodies are IgA. Some patients have an IgA deficiency. When you test for these antibodies, it is important to test for total Immunoglobulin A levels because if total IgA is low the coeliac test will be negative even when they have the condition.
Investigations must be carried out whilst the patient remains on a diet containing gluten otherwise it may not be possible to detect the antibodies or inflammation in the bowel.
Biopsy:
“Crypt hypertrophy”
“Villous atrophy”

23
Q

What is pysloric stenosis?

A

. Hypertrophy (thickening) and therefore narrowing of the pylorus is called pyloric stenosis. This prevents food traveling from the stomach to the duodenum as normal.
After feeding, there is increasingly powerful peristalsis in the stomach as it tries to push food into the duodenum. Eventually it becomes so powerful that it ejects the food into the oesophagus, out of the mouth and across the room. This is called “projectile vomiting”.

24
Q

Pyloric stenosis features?

A

Pyloric stenosis typically presents in the first few weeks of life, with a hungry baby that is thin, pale and generally failing to thrive. The classic description of vomiting you should remember for your exams is “projectile vomiting”.

If examined after feeding, often the peristalsis can be seen by observing the abdomen. A firm, round mass can be felt in the upper abdomen that “feels like a large olive”. This is caused by the hypertrophic muscle of the pylorus.

25
Q

Diagnosis and mx of pyloric stenosis?

A

Diagnosis is made using an abdominal ultrasound to visualise the thickened pylorus.

Treatment involves a laparoscopic pyloromyotomy (known as “Ramstedt’s operation“

26
Q

What is GORD?

A

In babies there is immaturity of the lower oesophageal sphincter, allowing stomach contents to easily reflux into the oesophagus. It is normal for a baby to reflux feeds, and provided there is normal growth and the baby is otherwise well this is not a problem

27
Q

Px of GORD?

A

Signs of problematic reflux include:

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

28
Q

What are some red flags in a gastro hx?

A

Not keeping down any feed (pyloric stenosis or intestinal obstruction)
Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)
Bile stained vomit (intestinal obstruction)
Haematemesis or melaena (peptic ulcer, oesophagitis or varices)
Abdominal distention (intestinal obstruction)
Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)
Respiratory symptoms (aspiration and infection)
Blood in the stools (gastroenteritis or cows milk protein allergy)
Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis)
Rash, angioedema and other signs of allergy (cows milk protein allergy)
Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment

29
Q

Mx of GORD?

A
  • Small freq meals and not overfeeding. Dont lie flat and burp baby
    More problematic cases can justify treatment with

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

30
Q

What is Sandifers syndrome?

A

This is a rare condition causing brief episodes of abnormal movements associated with gastro-oesophageal reflux in infants. The infants are usually neurologically normal. The key features are:

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
The condition tends to resolve as the reflux is treated or improves.

31
Q

What are some red flag sx for abdo pain in children?

A

Persistent or bilious vomiting
Severe chronic diarrhoea
Fever
Rectal bleeding
Weight loss or faltering growth
Dysphagia (difficulty swallowing)
Nighttime pain
Abdominal tenderness

32
Q

What Ix can be useful in finding the causes of abdominal pain in children?

A

Anaemia can indicate inflammatory bowel disease or coeliac disease
Raised inflammatory markers (ESR and CRP) can indicate inflammatory bowel disease
Raised anti-TTG or anti-EMA antibodies indicates coeliac disease
Raised faecal calprotectin indicates inflammatory bowel disease
Positive urine dipstick indicates a urinary tract infection

33
Q

What is abdominal migraine?

A

occur in young children before they develop traditional migraines as they get older. Abdominal migraine presents with episodes of central abdominal pain lasting more than 1 hour. Examination will be normal.

There may be associated:

Nausea and vomiting
Anorexia
Pallor
Headache
Photophobia
Aura

34
Q

How would you manage an abdominal migraine?

A

Treating the acute attack:

Low stimulus environment (quiet, dark room)
Paracetamol
Ibuprofen
Sumatriptan

35
Q

How would you prevent abdominal migraines?

A

Pizotifen is the main preventative medication to remember for abdominal migraine. It needs to be withdrawn slowly when stopping as it is associated with withdrawal symptoms such as depression, anxiety, poor sleep and tremor.
Pizotifen, a serotonin agonist
Propranolol, a non-selective beta blocker
Cyproheptadine, an antihistamine
Flunarazine, a calcium channel blocker

36
Q

What is encoparesis? What are some things that may cause it?

A

Encopresis is the term for faecal incontinence. This is not considered pathological until 4 years of age. It is usually a sign of chronic constipation where the rectum becomes stretched and looses sensation. Large hard stools remain in the rectum and only loose stools are able to bypass the blockage and leak out, causing soiling.

  1. Spinabifida, Hirschsprungs, cerebral palsy, stress and abuse
37
Q

Red flags for constipation?

A

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

38
Q

NICE recommendations for tackling constipation?

A

1.Correct any reversible contributing factors, recommend a high fibre diet and good hydration
2.Start laxatives (movicol is first line)
3.Faecal impaction may require a disimpaction regimen with high doses of laxatives at first
4.Encourage and praise visiting the toilet. This could involve scheduling visits, a bowel diary and star charts.

39
Q

What is the pathophysio of hirschsprungs?

A

key pathophysiology in Hirschsprung’s disease is the absence of parasympathetic ganglion cells. During fetal development these cells start higher in the GI tract and gradually migrate down to the distal colon and rectum. Hirschsprung’s occurs when the parasympathetic ganglion cells do not travel all the way down the colon, and a section of colon at the end is left without these parasympathetic ganglion cells.

40
Q

Presentation of hirschsprungs?

A

1.Delay in passing meconium (more than 24 hours)
2.Chronic constipation since birth
3.Abdominal pain and distention
4.Vomiting
5.Poor weight gain and failure to thrive

41
Q

What is HAEC?

A

Hirschsprung-associated enterocolitis (HAEC) is inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease. It typically presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis. It is life threatening and can lead to toxic megacolon and perforation of the bowel. It requires urgent antibiotics, fluid resuscitation and decompression of the obstructed bowel.

42
Q

What are the investigations and management of Hirschsprungs?

A

Abdominal X-ray , Rectal biopsy will often confirm the diagnosis - absence of ganglionic cells seen
Tx: fluid resus , IV abx, definitive mx is surgical removal of the aganglionic part of the intestine