Gastroenterology Flashcards

1
Q

medical causes of abdominal pain in children

A
  • Constipation
  • UTI
  • Coeliac disease
  • IBD
  • IBS
  • Mesenteric adenitis
  • Abdominal migraine
  • Pyelonephritis
  • Henoch-Schonlein purpura
  • Tonsilitis
  • DKA
  • Infant colic
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2
Q

causes of abdominal pain in adolescent girls

A
  • Dysmenorrhoea
  • Mittelschmerz
  • Ectopic preg
  • PID
  • Ovarian torsion
  • Pregnancy
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3
Q

surgical causes of abdominal pain in children

A
  • Appendicitis
  • Intussusception- colicky non specific abdo pain w/ redcurrent jelly stools
  • Bowel obstruction
  • Testicular torsion
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4
Q

what are some red flags for abdo pain in children

A
  • Persistent or bilious vomit
  • Severe chronic diarrhoea
  • Fever
  • Rectal bleeding
  • Weight loss or faltering growth
  • Dysphagia
  • Nighttime pain
  • Abdominal tenderness
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5
Q

what initial investigations may be done for abdominal pain in children and why?

A
  • Anaemia can indicate IBD or coeliac disease
  • Raised inflammatory markers can indicate IBD
  • Raised anti-TTG or anti- EMA antibodies can indicate coeliac
  • Raised faecal calprotectin IBD
  • Positive urine dip - UTI
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6
Q

what is recurrent abdo pain in children?

A

Repeated episodes of abdominal pain without identifiable cause. Non-organic or Functional. Common and can lead to psychological problems, such as missed days at school and parental anxiety. Overlap between diagnoses recurrent abdo pain, abdominal pain, IBS and functional abdominal pain.

Recurrent abdominal pain often responds to stressful life events, such as loss of a relative and bullying. Lead theory= increased sensitivity and inappropriate pain signals from visceral nerves.

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7
Q

how is recurrent abdominal pain managed in children?

A

Management= Careful explanation and reassurance. To help:

  • Distracting child from pain with other activities and interests
  • Encourage pt not to ask about or focus on the pain
  • Advice about sleep, reg meals, healthy balanced diet, staying hydrated, exercise and reducing stress
  • Probiotic substances may help IBS
  • Avoid NSAIDs
  • Address psychological triggers and exacerbating factors
  • Support from a school counsellor or child psychologist
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8
Q

what are abdominal migraines?

A

episodes of central abdominal pain lasting >1 hour

occur in children before they develop traditional migraines as they get older

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9
Q

what are some features of abdominal migraines?

A
  • Central abdominal pain lasting >1 hour
  • N&V
  • Anorexia
  • Pallor
  • Headache
  • Photophobia
  • Aura
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10
Q

how are abdominal migraines managed?

A
  • Low stimulus environment- quiet dark room
  • Paracetamol
  • Ibuprofen
  • Sumatriptan
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11
Q

what preventative measures for abdominal migraines can be used?

A
  • Pizotifen- serotonin agonist- withdraw slowly as associated withdrawal symptoms- depression, anxiety, poor sleep, tremor
  • Propanalol
  • Cyproheptadine- antihistamine
  • Flunarazine- CCB
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12
Q

what is idiopathic/functional constipation?

A

no significant underlying cause other than lifestyle factors

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13
Q

name 3 important secondary causes of constipation in children?

A

Hirschsprung’s disease

CF

hypothyroidism

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14
Q

how does constipation present in children?

A
  • <3 stools per week
  • Hard stools that are difficult to pass
  • Rabbit dropping stools
  • Straining and painful passing of stools
  • Abdominal pain
  • Holding an abnormal posture, referred to as retentive posturing
  • Rectal bleeding associated with hard stools
  • Faecal impaction causing overflow soiling, with incontinence of particularly loose smelly stools
  • Hard stools may be palpable
  • Loss of sensation of the need to open bowels
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15
Q

what is encopresis?

A

Term for faecal incontinence. Not considered pathological until 4 years of age. Usually, a sign of chronic constipation where the rectum becomes stretched and loses sensation. Large stools remain in the rectum and only loose stools able to bypass the blockage and leak out, causing soiling.

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16
Q

what are some lifestyle factors that impact constipation in children?

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 (keep safeguarding in mind)
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17
Q

describe desensitisation of the rectum

A

Habit of not opening bowels when they need to and ignoring the sensation of a full rectum= lose sensation overtime and open less frequently faecal impaction rectum stretches and desensitised= more difficult to treat and reverse problem

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18
Q

what are some secondary causes other than Hirschsprungs, CF and hypothyroidism?

A
  • Spinal cord lesions
  • Sexual abuse
  • Intestinal obstruction
  • Anal stenosis
  • Cows milk intolerance
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19
Q

what are some red flags for constipation?

A

no meconium w/in 48H birth (CF or Hirschsprung’s)

Neurological (cerebral palsy or spinal cord lesion)

Vomiting

ribbon stool

abnormal anus

abnormal lower back or buttocks

failure to thrive

Acute severe abdo pain and bloating

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20
Q

complications of constipation

A
  • Pain
  • Reduced sensation
  • Anal fissures
  • Haemorrhoids
  • Overflow and soiling
  • Psychosocial morbidity
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21
Q

how is constipation managed?

A

diagnosis of idiopathic constipation can be made without investigations, provided red flags are considered.

important to provide adequate explanation of the diagnosis and management as well as reassure parents about the absence of concerning underlying causes.

Explain that treating constipation can be a prolonged process, potentially lasting months.

  • Correct any reversible contributing factors, recommend high fibre+ good hydrate
  • Start laxatives (Movicol)
  • Impaction= disimpaction regimen with high doses laxatives at first
  • Encourage and praise visiting the toilet. This could involve scheduling visits, bowel diary and star charts.

Slow ween off as child develops a normal- regular bowel habit.

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22
Q

what are the 4 types of laxatives and name examples of each

A

stool softeners

stimulant laxatives

bulk forming agents

osmotic laxatives

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23
Q

what is GOR?

A

gastro oesophageal reflux

immaturity of the lower oesophageal sphincter

allows contents to easily reflux into oesophagus. Normal for baby to reflux feeds and provided there is normal growth, and the baby is otherwise well, there is no problem. Usually improves and 90% of infants stop having reflux by 1 year.

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24
Q

how does GOR present?

A

normal to have reflux with large feeds

problem when is causes them to be distressed

  • Chronic cough
  • Hoarse cry
  • Distress, crying or unsettles after feeding
  • Reluctance to feed
  • Pneumonia
  • Poor weight gain
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25
Q

what are some other causes fo vomiting in children?

A
  • Overfeeding
  • GORD
  • pyloric stenosis (projectile vomit)
  • gastritis or gastroenteresis
  • appendicitis
  • infection- UTI, tonsillitis or meningitis
  • Intestinal obstruction
  • Bulimia
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26
Q

what are some red flags for vomiting in children?

A
  • not keeping down any feed
  • projectile or forceful vomiting
  • bile stained, haematemesis or melaena
  • abdominal distension
  • reduced consciousness
  • bulging fontanelle or neuro signs (meningitis or raised ICP)
  • respiratory symptoms
  • blood in stools (gastroenteritis or cows milk protein allergy)
  • signs infection, rash/angioedema- sign allergy
  • Apnoea
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27
Q

how is GOR managed?

A
  • small frequent meals
  • burping to help settle milk
  • not over-feeding
  • keep baby upright when feeding
  • more problematic:
    • gaviscon mixed with feeds
    • thickened milk/formula
    • Ranitidine
    • Omeprazole where ranitidine inadequate

rare severe cases - barium meal and endoscopy

surgical fundoplication can be considered in v severe cases but rarely done

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28
Q

what is Sandifer’s syndrome?

A

RARE condition causing brief episodes of abnormal movements associated w/ GORD in infants. Usually neurologically normal.

Features:

  • Torticollis- forceful contraction of the neck muscles when twisting the neck
  • Dystonia- abnormal muscle contractions causing twisting movements, arching of the back and unusual postures.

Tends to resolve as the reflux is treated or improves. Generally, the outcome is good.

refer to specialist for assessment as DDx include infantile spasms aka west syndrome and seizures

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29
Q

what is pyloric stenosis?

A

pyloric sphincter is ring of smooth muscle that forms canal between stomach and duodenum

it can hypertrophy and become narrowed = stenosis

powerful peristalsis to push feed into duodenum but cant pass through stenosis so peristalsis causes projectile vomiting

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30
Q

what are some features of pyloric stenosis

A
  • Thin
  • Pale
  • Failing to thrive
  • Projectile vomiting
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31
Q

what can be seen on examination of a baby with pyloric stenosis?

A

after feeding - peristalsis can be seen by observing the abdomen

firm round mass can be felt in upper abdomen

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32
Q

what ABG finding will be present in pyloric stenosis?

A

hypochloric hypokalemic metabolic alkalosis due to vomiting HCL

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33
Q

how is pyloric stenosis diagnosed?

A

abdominal uss to visualise thickened pyloric sphincter

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34
Q

how is pyloric stenosis managed?

A

laparoscopic pyloromyotomy - Ramstedts’s operation

inscision made through the SM of the pylorus to widen canal allowing for food to pass from stomach to duodenum as normal

prognosis is good

baby cab feed after 6 h

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35
Q

what is coeliac disease?

A

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

Usually develops in early childhood but can start any age.

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36
Q

what are the 2 main antibodies involved?

A

anti-tissue transglutaminase (anti- TTG) and anti-endomysial (anti-EMA)

they correlate to disease activity and may disappear with effective treatment

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37
Q

what is the pathophysiology of coeliac disease?

A

Inflam SI especially the jejunum. Causes atrophy intestinal villi. Inflam- malabsorption of nutrients and disease related symptoms.

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38
Q

how does coeliac 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

Rarely can present w/ neurological symptoms:

  • Peripheral neuropathy
  • Cerebellar ataxia
  • Epilepsy
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39
Q

patients newly diagnosed with what condition are also tested for ceoliac and why?

A

type 1 DM as heavily linked

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40
Q

what are some genetic associations with coeliac?

A

HLA - DQ2 gene

HLA - DQ8 gene

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41
Q

what antibodies are involved? and what is the significance of IgA abs?

A
  • Tissue transglutaminase antibodies (anti-TTG)
  • Endomysial antibodies (EMAs)
  • Deaminated gliadin peptides antibodies (anti-DGPs)

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. In this circumstance you can test for the IgG version of the anti-TTG or anti-EMA antibodies or do an endoscopy with biopsies.

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42
Q

how is coeliac disease diagnosed?

A

investigatiosn must be carried out whilst person is still eating gluten

check total IgA levels to exclude IgA deficiency before checking coeliac disease specific antibodies

endoscopy and intestinal biopsy will show crypt hypertrophy and villous atrophy

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43
Q

what conditions are associated with coeliac disease?

A
  • Type 1 diabetes
  • Thyroid disease
  • Autoimmune hepatitis
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • Down’s syndrome
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44
Q

what are some complications of untreated coeliac disease?

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-Hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
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45
Q

how is coeliac disease managed?

A

Lifelong gluten free diet essentially curative. Checking antibodies can be helpful in monitoring disease

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46
Q

what is biliary atresia?

A

Congenital condition where a section of the bile duct is either narrowed or absent. Results in cholestasis. Conjugated bilirubin is excreted in bile and therefore biliary atresia stops this.

Presents shortly after birth.

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47
Q

how does biliary atresia present?

A
  • Shortly after birth
  • Sig jaundice due to high conjugated bilirubin levels - liver is processing but cant be excreted
  • Persistent jaundice >14 days in term babies and 21days in premature babies
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48
Q

what investigations are done for ? biliary atresia?

A

Conjugated and unconjugated bilirubin.

high proportion of conjugated bilirubin suggests that the liver is processing it but it is unable to be excreted

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49
Q

how is biliary

A

Surgery- Kasai portoenterostomy involves attaching a section of 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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50
Q

what is intestinal obstruction?

A

blockage in the bowel

back pressure - vomiting and absolute constipation

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51
Q

causes of intestinal obstruction?

A

meconium ileus

Hirschsprung’s disease

Oesophageal atresia

Duodenal atresia

intussusception

imperforate anus

malrotation of intestines= volvulus

Strangulated hernia

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52
Q

how does intestinal obstruction present?

A
  • Persistent vomiting, may be bilious containing bright green bile
  • Abdo pain and distension
  • Failure to pass stools or wind
  • Abnormal bowel sounds. Can be high pitched and tinkling early in obstruction but absent later
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53
Q

how is intestinal obstruction diagnosed?

A

AXR may show dilated loops of bowel proximal to obstruction and absence of air in the rectum

(fluid level= Hirchsprungs and none= Meconium ileus)

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54
Q

how is intestinal obstruction managed?

A
  • paediatric surgical unit as an emergency
  • them NBM and inserting NGT to help drain stomach and stop vomiting.
  • Also require IVF to correct electrolyte imbalance and keep them hydrated
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55
Q

what is hirschsprungs disease?

A

Congenital condition where the nerve cells of the myenteric plexus are absent in the distil bowel and rectum. Myenteric plexus aka Auerbach’s plexus forms enteric nervous system, brain of the gut. Responsible for peristalsis of large bowel (circular muscle layer).

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56
Q

pathophys of hirchsprung’s disease?

A

absence of parasympathetic ganglion cells as in embryology these cells start higher up in GI tract and migrate down and if don’t travel all the way down, then part of the bowel left without any parasympathetic ganglion cells = Hirschsprung’s.

Length of colon without innervation varies:

  • When entire= total colonic aganglionosis.
  • Part w/o innervation= does not relax and becomes constricted= obstruction

Submucosa- Meissner’s plexus- secretion and blood flow

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57
Q

what are some genetic associations of hirschsprungs disease

A

family hx

downs syndrome

neurofibromatosis

Waardenburg Syndrome

multiple endocrine neoplasia type II

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58
Q

how does hirschsprung’s disease present?

A

Severity of presentation and the age at diagnosis varies significantly depending on individual and amount of bowel affected. Acute intestinal obstruction after birth or gradual

  • >24H delay in passing meconium
  • Chronic constipation since birth
  • Abdo pain and distention
  • Vomiting
  • Poor weight gain and failure to survive
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59
Q

what is hirschsprung-associated enterocolitis?

A

Inflam and obstruction of intestine occurring in around 20% neonates with the disease.

Typically presents w/in 2-4 weeks of birth w/ fever, abdo distension, diarrhoea (often w/ blood) and features of sepsis.

Life threatening and can lead to toxic megacolon and perforation of the bowel.

Requires ABX, fluid resuscitation and decompression of obstructed bowel.

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60
Q

how is hirschsprungs investigated?

A

AXR can be helpful in diagnosing intestinal obstruction and demonstrating features HAEC

Rectal biopsy is used to confirm the diagnosis.

Bowel histology = absence of ganglionic cells.

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61
Q

how is hirschsprung’s disease managed?

A

unwell and those with enterocolitis - IVF and management like obstruction

definitive management is by surgical removal of aganglionic section of bowel.

Most live normal life after corrective surgery, although they can have long term disturbances in bowel function and may be left with some degree of incontinence.

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62
Q

what is intersussception?

A

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

Thickens bowel and narrows lumen, leading to a palpable mass in the abdomen and obstruction to the passage of faeces through the bowel.

Typically occurs in infants 6 months to 2 years and is more common in boys.

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63
Q

what are some associated conditions with intussusception?

A
  • Concurrent viral illness
  • Henoch- Schonlein purpura
  • CF
  • Intestinal polyps
  • Meckel diverticulum
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64
Q

how does intussusception present?

A
  • Severe colicky abdominal pain
  • Pale, lethargic, and unwell child
    • Redcurrant jelly stool
  • RUQ mass on palpation- sausage shaped
  • Vomiting
  • Intestinal obstruction
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65
Q

what is the initial investigation of choice for intussusception?

A

USS or contrast enema

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66
Q

how is intussusception managed?

A

Therapeutic enemas can be used to try and reduce intussusception.

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

Surgical reduction may be necessary if enemas don’t work

If gangrenous or perforated surgical resection is required

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67
Q

what are some complications of intussusception?

A
  • Gangrenous Bowel
  • Obstruction
  • Perforation
  • Death
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68
Q

what is appendicitis?

A

Appendix is a small, this tube sprouting from the caecum. Becomes inflamed due to infection trapped in the appendix by obstruction at the point where the appendix meets the bowel. Inflammation can quickly proceed to gangrene and rupture. The appendix can rupture and release faecal content and infective material = peritonitis.

Peak incidence 10-12y/o

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69
Q

what are the clinical features of appendicitis?

A
  • Migratory abdominal pain from central to RIF- tenderness McBurney’s point (1/3rd distance ASIS to umbilicus.
  • Loss appetite
  • N&V
  • Rovsing’s sign- palpation LIF causes pain RIF
  • Guarding on abdominal palpation
  • Rebound tenderness
  • Percussion tenderness

Rebound tenderness and percussion tenderness are signs of peritonitis from a ruptured appendix.

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70
Q

how is appendicitis diagnosed?

A

Clinical presentation and raised inflammatory markers

USS F patients to exclude ovarian and gynaecological pathology

CT scan

Clinical presentation but -ve investigations= Diagnostic laparoscopy to visualise appendix

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71
Q

key ddx for appendicitis?

A

ectopic preg

ovarian cyst

meckles diverticulum

mesenteric adenitis

appendix mass

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72
Q

what is an appendix mass?

A

occurs when the omentum surrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa.

This is typically managed conservatively with supportive treatment and antibiotics, followed by appendicectomy once the acute condition has resolved.

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73
Q

how is appendicitis managed?

A

Emergency admission to hospital under surgical team.

Older children, >10y/o can often be managed by adult teams provided there is a paediatric department in the hospital.

Younger= paed surgeons

Appendicectomy is definitive- laparoscopy or laparotomy

74
Q

what are some complications of appendicectomy?

A
  • Bleeding, infection, pain and scars
  • Damage to bowel, bladder and other organs
  • Removal of a normal appendix
  • Anaesthetic risks
  • VTE risk
75
Q

what is hepatitis?

A

inflammation of the liver

76
Q

what causes hepatitis?

A

alcoholic, NAFLD, autoimmune, drug induced ie paracetamol

77
Q

how does hepatitis present?

A
  • Abdominal Pain
  • Fatigue
  • Pruritis
  • Muscle and joint aches
  • N&V
  • Jaundice
  • Fever (VIRAL)
  • Hepatic picture LFT
78
Q

what is the typical biochemical findings for hepatitis?

A

LFT deranged

high transaminases with proportionally less of a rise in ALP = hepatic picture

79
Q

what is hepatitis A?

A

most common viral hepatitis in world - rare in UK

RNA virus transmitted via faecal=oral route by contaminated water/faeces

presents with nausea, vomiting, anorexia & jaundice

can cause cholestasis = dark urine and pale stools, moderate hepatomegaly

resolves without treatment in 1-3 months

basic analgesia

vaccination

notifiable disease

80
Q

what is hepatitis B?

A

DNA virus transmitted by direct contact with blood or bodily fluids - sex, sharing household products, contact between cuts/abrasions

also vertical transmission

fully recover within 2 months - 10% become chronic hep b carriers - will cont. to produce viral proteins

81
Q

hepatitis B antibodies

A
  • Surface antigen (HBsAg) – active infection
  • E antigen (HBeAg) – marker of viral replication and implies high infectivity
  • Core antibodies (HBcAb) – implies past or current infection
  • Surface antibody (HBsAb) – implies vaccination or past or current infection
  • Hepatitis B virus DNA (HBV DNA) – this is a direct count of the viral load
82
Q

vaccination for Hep B

A

Part of the 6 in 1 vaccine

83
Q

how is hep b managed?

A
  • Low threshold to screen
  • Screen BBV- A, B, HIV and STI
  • Refer gastro, hepatology or ID and PHE
  • Stop smoke and alcohol
  • Education about reducing transmission and informing potential risk contacts
  • Test Complications- Fibroscan for cirrhosis and USS for hepatocellular carcinoma
  • Antiviral medication can be used to slow progression of the disease and reduce infectivity
  • Liver transplant in end stage disease.
84
Q

what is hepatitis C?

A

RNA virus. Spread by blood and bodily fluids. No vaccine available and now curable by direct antiviral medications.

COURSE

  • 1in4 fights off and makes full recovery
  • 3in4 becomes chronic
  • Complications- Liver cirrhosis and associated complications and hepatocellular carcinoma

Testing- HepCab and HepC RNA to calculate viral load and assess for individual genotype

85
Q

how is hepatitis c managed?

A
  • Same as B
  • Direct acting antiviral tailored to specific genotype. Successful in 90% and taken 8-12 weeks
  • Transplant end stage
86
Q

what is hepatitis D?

A

RNA virus- only pt with HepB as attaches itself HBsAG. Very low rates UK. No treat and notify PHE

87
Q

what is hepatitis E?

A

RNA virus transmitted faecal oral. VERY RARE. Mild illness, no treatment required. Rarely chronic and liver fail and more so in immunocomp. Notifiable PHE. No vaccination.

88
Q

what is autoimmune hepatitis?

A

Chronic hepatitis not sure exact cause however could be some genetic predisposition and triggered environmental, such as viral infection = T cell- mediated response against liver cells.

Type 1:adults

Type 2: occurs children

Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

89
Q

what investigations are done for autoimmune hepatitis?

A

Raised transaminases, IgG levels and it is associated with many autoantibodies.

T1 autoantibodies = ANA, Anti-smooth muscle ab (anti-actin), Anti-soluble liver antigen (anti- SLA/LP

T2 autoantibodies = Anti-liver kidney microsomes-1 (Anti-LKM1), Anti-liver cytosol antigen type 1 (anti-LC1)

Diagnosis can be confirmed in a liver biopsy

90
Q

how is autoimmune hepatitis managed?

A

High dose prednisolone that are tapered over time as other immunosuppressants, particularly azathioprine are introduced.

Immunosuppressant treatment is usually successful in inducing remission however usually lifelong.

Liver transplant end stage although can recur

91
Q

what are some symptoms of liver failure?

A
  • Malaise
  • Abdominal pain
  • Nausea ± vomiting
  • Weight loss
  • Jaundice
92
Q

what are some signs of liver failure?

A
  • Bruising and bleeding – signs of coagulopathy
  • Hypoglycaemia
  • Oedema
  • Loss of consciousness
  • Irritability
  • Drowsiness
93
Q

ddx/causes for liver failure

A
  • Infection – hepatitis, CMV, EBV, parvovirus B19, herpes simplex
  • Drugs – paracetamol, anticonvulsants
  • Autoimmune
  • Metabolic – Wilson’s disease
  • Ischaemia – congenital heart disease
  • Malignancy – leukaemia
94
Q

what investigations can be done for liver failure?

A
  • Bloods – FBC, coagulation screen, G&S, U&Es, creatinine, LFTs, CRP
  • Blood sugar levels
  • Blood gas
  • Lactate
  • Ammonia
  • Amylase
  • EEG or CT if grade 2 encephalopathy or higher
  • Abdominal USS
  • CXR
  • ECG
95
Q

how is paediatric acute liver failure defined?

A

biochemical evidence of acute liver injury in a child, with no known evidence of chronic liver disease and at least 1 of the following:

  • INR >1.5 with encephalopathy
  • INR >2.0 without encephalopathy
96
Q

how is liver failure managed?

A
  • IV omeprazole
  • IV vitamin K
  • PO/NG lactulose- reduce ammonia in blood
  • IV Cefazolin (B lactam ABX)
  • Analgesia
  • Avoid sedating medications

Indications for admission to ITU include:

  • Grade 2 encephalopathy or higher
  • Cardiovascular or respiratory instability
  • Multiorgan failure
97
Q

what is peptic ulcer disease?

A

ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer).

Duodenal ulcers are most common.

98
Q

what is the pathophysiology of peptic ulcer disease?

A

protective layer in the stomach comprised of mucous and bicarbonate secreted by the stomach mucosa. This protective layer can be broken down by:

  • Medications (e.g. steroids, NSAIDs)
  • H. pylori
99
Q

what are the clinical features of peptic ulcers?

A
  • Epigastric discomfort/pain – eating worsens the pain of gastric ulcers, and improves the pain of duodenal ulcers
  • Nausea ± vomiting
  • Dyspepsia
  • Haematemesis
  • Iron deficiency anaemia
100
Q

what are some ddx for peptic ulcer disease?

A

Crohn’s disease, Oesophagitis, Cholecystitis

101
Q

how is peptic ulcer disease investigated?

A
  • Endoscopy
  • Rapid urease test – to check for H. pylori
  • Stool tests
  • Biopsy – exclude malignancy
102
Q

how is peptic ulcer disease managed?

A
  • High-dose PPI
  • H. pylori eradication regime
103
Q

complications of peptic ulcer disease?

A
  • Haemorrhage
  • Perforation – peritonitis
  • Strictures
  • Pyloric stenosis
104
Q

what is gastritis?

A

inflammation or irritation of the lining of the stomach?

105
Q

what are some causes of gastritis?

A
  • Toxic object swallowed
  • Trauma to the stomach
  • NSAIDs
  • DM
  • Thyroid disease
  • Crohn’s disease
106
Q

what are the clinical features of gastritis in infants and young children?

A
  • Vomiting
  • Failure to thrive
  • Weight loss
  • Chronic diarrhoea
  • Haematemesis
  • Iron-deficiency anaemia
  • Irritability
107
Q

what are the clinical features of gastritis in children and adolescents?

A
  • Abdominal pain
  • Anorexia
  • Nausea ± vomiting
  • Heartburn
  • Hematemesis
  • Iron-deficiency anaemia
108
Q

what investigations are done for gastritis?

A

bloods

stool test

urease breath test

endoscopy

109
Q

how is gastritis managed?

A
  • High-dose PPI Ranitidine before
  • H. pylori eradication regime
110
Q

what is h. pylori and how is it eradicated?

A

a gram -ve bacteria. Urease producing.

Eradication can be achieved with a 7-day course of:

  • PPI + amoxicillin + clarithromycin/metronidazole
  • PPI + metronidazole + clarithromycin (if penicillin allergic)
111
Q

what is volvulus?

A

when the bowel and its mesentery twist around itself

Mesentery= membranous peritoneal tissue that creates a connection between the bowel and the posterior abdominal wall.

Closed-loop bowel obstruction.

Can cause ischaemia and bowel necrosis.

112
Q

what are the different types of volvulus?

A

Sigmoid (older, bed bound, key cause= constipation= lengthen mesentery causing it to go down and twist, also associated with a high fibre diet and the excessive use of laxatives)

Caecal- less common and tends to affect younger patients. Twist occurs in the caecum.

113
Q

risk factors for volvulus

A

neuropsych disorders (Parkinsons), Nursing home residents

chronic constipation

high fibre diet

pregnancy

Adhesions

114
Q

how does volvulus present?

A
  • Vomiting (particularly green bilious vomit)
  • Abdominal distension
  • Diffuse abdominal pain
  • Absolute constipation and lack of flatulence
115
Q

how is volvulus diagnosed?

A

Diagnosis= coffee bean sign in sigmoid volvulus

Contrast CT

116
Q

how is volvulus managed?

A

NBM, NGT, IVF

Conservative management with endoscopic decompression can be attempted in pt with sigmoid volvulus.

Flexible sigmoidoscope is inserted carefully, with the patient in the left lateral position, resulting in correction of the volvulus. A flatus tube/rectal tube placed temporarily to help decompress the bowel and is later removed.

60% risk recurrence

Surgical:

  • Laparotomy
  • Hartmann’s
  • Ileocecal resection or right Hemicolectomy for caecal volvulus
117
Q

what is peritonitis?

A

Inflammation of the peritoneum and can have localised with inflammation of the underlying organ

M>W, In women they can occur with rupture to reproductive organs

118
Q

what are symptoms of peritonitis?

A
  • Sudden onset acute abdominal pain exacerbated by movement
  • Generalised but then become localised visceralparietal
  • Shock and fever
  • Washboard rigidity
  • Fever
  • Sinus tachycardia
  • N&V
  • Abdominal swelling
  • Dullness may occur after 2-4H
119
Q

what are some causes of peritonitis?

A
  • Infected peritonitis- perf= gram -VE (E.Coli), surgery or trauma (staph aureus), SBP in children or those with ascites. Treated differently and normally only requiring abx, systemic infection=TB
  • Non-infected= leakage of sterile bodily fluids into the peritoneum- bld bile, urine- sterile to start but then bacterial in 24-48H= full blown peritonitis
  • Auto-immune disease- lupus can cause peritonitis
120
Q

how is peritonitis investigated?

A

erect CXR

serum amylase to rule out pancreatitis

USS/CT scan

121
Q

how is peritonitis managed?

A

IVF

IVABX if infective

Surgery= laparotomy- if normal urine output attained. Repair perf and washout. Antibiotic wash

Left untreated= fatal

Easily treated surgically= mortality<10% and rise 40% in elderly

Later present= likely fatal consequences, particularly those after 48H

After surgery= IV feed

122
Q

what are some complications of peritonitis?

A

Loss fluids/electrolyte imbalance

Difficulty breathing

Peritoneal abscess

Septicaemia

Abscess

123
Q

what is duodenal atresia and stenosis?

A

first part of the small bowel (the duodenum) has not developed properly. It is not open and cannot allow the passage of stomach contents.

associated with HPB anomalies

124
Q

what are some clinical features of duodenal atresia?

A
  • Intrauterine polyhydramnios
  • Bilious vomiting- severe= few hours after birth
  • Distended upper abdomen and scaphoid lower abdomen
  • Delayed meconium
125
Q

how is duodenal atresia diagnosed?

A
  • Prenatal USS- polyhydramnios, dilation of stomach and duodenum= double bubble sign
  • Postnatal XR- double bubble, gasless distil bowel
126
Q

how is duodenal atresia managed?

A

Preoperative- PN via central catheter shortly after birth and fluids for electrolyte replacement and hydration.

Also Gastric decompression.

Surgical bypass of atresia or stenosis - Duodenoduodenostomy

127
Q

what is an omphalocele?

A

Ventral abdominal wall defect- congenital herniation of abdominal viscera through the abdominal wall at the umbilicus

Hernial sac covered in amniotic membrane and peritoneum

Impaired closure of the umbilical folds.

128
Q

what are some risk factors for omphalocele?

A

m>f

trisomy 21, 18, 13

Beckwidth-Weidemann Syndrome

129
Q

what are the clinical features of omphalocele?

A
  • premature infants
  • Umbilical hernia sac- May contain liver, gall bladder, intestine
  • Features of associated conditions
130
Q

how is omphalocele diagnosed?

A

clinical diagnosis at birth

prenatal uss - polyhydramnios and high maternal serum AFP

131
Q

how is omphalocele managed?

A

C-section to avoid rupture

Vaginal delivery possible if small

Wrap sac in sterile saline dressing covered with plastic wrap

NG suction

IVF to avoid abdo distension to compensate fluid loss

Surgery- prim closure or secondary (staged silo repair, skin graft or dermal patch)

132
Q

what are some complications of omphalocele?

A

Rupture hernial sac with infection-peritonitis

Secondary intestinal wall atresia as a result of injury

133
Q

What is gastroschisis?

A

Ventral wall defect that results in paraumbilical herniation of the intestine through the abdominal wall without formation of a hernia sac.

Failed formation of a large peritoneal cavity=rupture or fail return

134
Q

what are the clinical features of gastroschisis?

A

Protrusion of intestinal content usually on the right side of umbilicus

Not contained in a hernia sac and appears edematous, erythematous and dull

Shortened bowel

Malabsorption caused by mucosal damage

Peritonitis

Seen especially in premature infants and associated cryptorchidism and GI stenoses or atresia

135
Q

how is gastroschisis diagnosed?

A

Clinical diagnosis

Can be detected prenatally like omphalocele

136
Q

how is gastroschisis managed?

A

C section no better than a vaginal delivery

Same as omphalocele

Emergency surgery- Prim abdo wall closure or staged silo repair

137
Q

what is a transoesophageal fistula?

A

congenital anomaly resulting in a tract between trachea and oesophagus

138
Q

what is transoesophageal fistula associated with?

A

VACTERL anomalies

vertebral, anal, cardiac, tracheal, oesophageal, renal, limb defects

139
Q

how does a transoesophageal fistula present?

A

Increased oral secretions- drooling

Feeding difficulty

Gagging/choking

Hyperventilation or other resp dysfunction

140
Q

what is seen on examination of transoesophageal fistula?

A

Resp distress

Polyhydramnios in utero

Rales on pulmonary auscultation

Cyanosis

Abdo distension- caused by swallowing air during feeding

141
Q

what imaging is done for transoesophageal fistula?

A

CXR- may show NG coiled oesophagus

KUB- Air GI tract

Bronchoscopy- confirms anatomical abnormality

Prenatal USS- polyhydramnios

142
Q

how is transoesophageal fistula managed?

A

Surgical= repair- emergency when identified as prevents further lung damage

143
Q

what are some complications of transoesophageal fistula

A

Aspiration pneumonia

Choking

Oesophageal stricture post op

Reflux post op

144
Q

what is meckel’s diverticulum?

A

Congenital anomaly of the Gi tract and is caused by an incomplete obliteration of the omphalomesenteric duct.

145
Q

what is the rule of 2s for meckels diverticulum?

A

2 inches long

2 feet from the ileocaecal valve

2% pop

2:1 M:F

presents <2yrs with painless lower GI bleeding.

2 types of mucosa - native ileal or ectopic (most common) could be gastric, pancreatic etc

146
Q

what are some clinical features?

A

Asymptomatic- most common and an incidental finding in abdominal surgery

Symptomatic:

  • Lower GI bleeding= Haematochezia, Tarry stool, Currant Jelly stools
  • Abdominal pain
  • N&V
147
Q

what imaging is done for meckels diverticulum?

A

Lower GI bleed- <10y/o, adults with no abnormalities on endoscopy, colonoscopy, CTscan

Meckel scintigraphy- non-invasive nuclear medicine technique, which is absorbed by the gastric mucosa and identify ectopic gastric mucosa

CT angio

OTHER- Mesenteric angiography, Tagged RBC scans

NEW= double balloon enterostomy to visualise entire small bowel.

Capsule endoscopy

Diagnostic laparoscopy

148
Q

how is meckels diverticulum managed?

A

Asymp:

  • Children or young adults= resect
  • Adult<50= surgical resect high risk complications
  • Adults>50 no treatment necessary

Symptomatic or complicated:

  • Initial stabilisation of the pt, Surgical resection of all symptomatic/complicated
  • Procedures- segmental resection (indicated for bleeding, broad base or palpable abnormality) or diverticulectomy
149
Q

what are some complications of meckels diverticulum?

A

Haemorrhage

Bowel obstruction- intussusception, volvulus, Littre hernia: incarceration of Meckel diverticulum inside femoral hernia.

Bowel perf, peritonitis, intra-abdominal abscess

Infection

Neoplasia-rare- leiomysarcomas, carcinoid tumours, lipomas, fibromas, angiomas

150
Q

complications of malrotation?

A

volvulus

151
Q

what is a hiatus hernia?

A

Protrusion of a whole or part of an organ through the wall of the cavity that contains it into abnormal position. Extremely common, however exact prevalence hard to state. 1/3rd over 50 have a hiatus hernia.

152
Q

what are the 2 types of hiatus hernia?

A
  • Sliding Hiatus Hernia (80%)- GOJ, the abdo part of the oesophagus, and freq the cardia of the stomach slides upwards through the diaphragmatic hiatus into thorax
  • Rolling or para-oesophageal- upward movement of the gastric fundus occurs to lie alongside a normally positioned GOJ= create a bubble of the stomach. True hernia with peritoneal sac.
153
Q

what are some risk factors for hiatus hernia?

A

age - loss of diaphragmatic tone

pregnancy

obesity

ascites

154
Q

what are the clinical features of hiatus hernia?

A

Asymp

  • Reflux
  • Vomiting
  • Weight loss
  • Bleed or anaemia
  • Hiccups or palpitations
  • Swallowing difficulties
  • Clinical exam normal
155
Q

what investigations are done for hiatus hernia?

A

OGD gold standard

Diagnosed incidentally CT or MRI

156
Q

what is the management of hiatus hernias?

A

Conservative- PPI, weight loss and alteration of diet (low fat, earlier meals, smaller portions)

Smoking cessation and reduction in alcohol intake should be advised, as both nicotine and alcohol are thought to inhibit LOS function, thereby worsening symptoms.

Surgical Management

Indicated when:

  • Remaining symptomatic, despite max therapy
  • Increased risk of strangulation/volvulus
  • Nutritional failure (gastric outlet function)

Cruroplastly- hernia is reduced- large defects require mesh to strengthen repair

Fundoplication- Strengthen LOS and helping reflux and keep the GOJ in place below the diaphragm- wrap full or partial

157
Q

what are the complications of hiatus hernia?

A

Rolling= incarceration and strangulation

Gastric volvulus when twists on itself= obstruct gastric passage and tissue necrosis and requires prompt surgical intervention

158
Q

what is Borchardts triad - acute gastric volvulus?

A

severe epigastric pain

retching w/o vomiting

inability to pass NG tube

159
Q

what is an inguinal hernia?

A

Protrusion of a viscus through the wall of the cavity that contains it

  • Direct=20%= Hesslebachs triangle- older and secondary to abdo wall laxity and increase abdo pressure.
  • Indirect= 80%= Deep inguinal ring= incomplete closure processes vaginalis from vesicular descent- lat to epigastric vessels

Deep ring is transverse fascia. Superficial ring= external oblique

160
Q

what are some risk factors for hernia?

A

male

increased age

increased abdo pressure

obesity

161
Q

clinical features of inguinal hernia?

A
  • Lump in the groin
  • Mild/mod discomfort when activity or stand
  • Incarcerated=pain, tender, erythematous
  • Bowel ob= if reducible, V painful out clinical picture= strangulated-X blood= tense tender lump
  • Cough impulse- irreducible= no
  • Location= inguinal superomedial to pubic tubercule. Femoral inferolateral to pubic tubercule
  • Reducible = on lying down +/- minimal pressure
  • Testes above, separate?
162
Q

how is inguinal hernia investigated?

A
  • Imaging if not sure
  • USS-CT
163
Q

how is an inguinal hernia managed?

A

risk strangulate 3%

  • Strangulated- urgent surgical intervention
  • No symptoms= conservative- safety net and likely surgery future
  • Symptomatic= surgery after

Surgery

Open repair (++ cost effective prim inguinal)- Lichentein technique or laparoscopic total extra peritoneal (TEP) or transabdo pre-peritoneal TAP

URGENT= incarcerated, obstruct, strangulate

164
Q

what are some complications of inguinal hernia?

A

Pain, bruise, haematoma

Recurrence

Chronic pain

Damage vas or test vessels- ischaemic orchitis or test vessels

165
Q

why are femoral hernias higher risk for strangulation?

A

narrow femoral canal and ring

166
Q

what are the clinical features of femoral hernia?

A
  • Small lump groin= only or strangulation
  • How exactly location
  • Unlikely reducible
  • Older F+ vom= examine groin
167
Q

what investigations are done for femoral hernias?

A

uss

CT abdo pelvis

all for surgical intervention

168
Q

how are femoral hernias managed?

A
  • Low approach= incision below inguinal ligament= not interfering inguinal structures but limit space removal small bowel
  • High approach= above inguinal lig= preferred emergency= easy access compromised small bowel
  • Reduce+narrow femoral ring w/ sutures medially between the pectineal and inguinal ligaments or mesh plug
  • Emergency= incarcerated, obstructed, strangulated
169
Q

what is mesenteric adenitis?

A

an important cause of right iliac fossa pain in children, and as such is important as a differential diagnosis of appendicitis.

due to non- specific inflammation of the mesenteric lymph nodes which provokes a mild peritoneal reaction and stimulates painful peristalsis in the terminal ileum.

170
Q

what causes mesenteric adenitis?

A

infection - usually viral

common in under 16

171
Q

what are the symptoms of mesenteric adenitis?

A
  • Sore throat or symptoms of a cold before the tummy pain started
  • Pain in the tummy. Pain is usually in the middle of the abdomen. May be RIF pain
  • Fever
  • Nausea and/or diarrhoea
172
Q

how is mesenteric adenitis diagnosed?

A

exclude other causes ie appendicitis

  • Wait and see, with another check by your doctor a few hours later to see if symptoms have changed
  • Second opinion- eg, a referral for surgical opinion
  • Tests to look for other conditions
  • Blds, Urine dip, USS or CT.
  • May need laparoscopy
173
Q

how is mesenteric adenitis managed?

A

Analgesia if required

Bacterial infection= need abx

RED FLAG Safety netting

174
Q

what is gastroenteritis?

A

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

175
Q

what is the most common cause of gastroenteritis?

A

viral

176
Q

what is the main concern with patients with gastroenteritis?

A

dehydration - need to establish whether they can keep themselves hydrated or if they need IVF

177
Q

what are some conditions to think about when a child presents with loose stools?

A
  • Infection (gastroenteritis)
  • Inflammatory bowel disease
  • Lactose intolerance
  • Coeliac disease
  • Cystic fibrosis
  • Toddler’s diarrhoea
  • Irritable bowel syndrome
  • Medications (e.g. antibiotics)
178
Q

what are the 2 most common viral gastroenteritis?

A

rotavirus

norovirus

(adenovirus is less common and more subacute diarrhoea)

179
Q

describe the different causes of gastroenteritis

A
180
Q

how is gastroenteritis managed?

A

good hygiene

barrier nurse

stay off school 48 hours after symptoms have completely resolved

microscopy, culture and sensitivities to establish cause and need for abx

ensure hydration - fluid challenge, rehydration sachets

dehydrated or those who fail fluid challenge may need IVF

once oral intake is tolerated light diet can be started - toast is good to start

antidiarrhoeal and antiemetic medication are avoided

abx for those at high risk

181
Q

what are some long term complications of gastroenteritis?

A
  • Lactose intolerance
  • Irritable bowel syndrome
  • Reactive arthritis
  • Guillain–Barré syndrome