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NP- Phase 3a Medicine > paeds- GI > Flashcards

paeds- GI Flashcards

1
Q

causes of gastroenteritis in children

A

rotavirus

norovirus

astrovirus

adenovirus

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2
Q

risk factors for gastroenteritis

A
  • poor hygiene
  • compromised immune system
  • poorly cooked food = may lead to infection
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3
Q

clinical presentation of gastroenteritis

A
  • sudden onset of diarrhoea/ vomiting
  • pain
  • complications- dehydration, malnutrition, intolerance to sugar
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4
Q

what tests would be done in a patient presenting with gastroenteritis?

A

stool sample- bacteria, ova, cysts, parasites

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5
Q

how is gastroenteritis managed?

A
  • correct dehydration
  • oral rehydration therapy
  • IV therapy
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6
Q

what is a common complication of gastroenteritis and how is it managed?

A

transient lactose intolerance

managed via removal of lactose from diet for a few months followed by gradual reintroduction

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7
Q

describe colic in paediatric patients

A

paroxysmal crying with pulling up of the legs- for over 3 hours at least 3 days of the week for at least 3 months

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8
Q

how is a cows milk allergy confirmed?

A

confirmed with cows milk challenge- skin prick test and IgE antibodies in blood (RAST test)

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9
Q

what immunoglobulins is cows milk allergy associated with?

A

IgG , IgE

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10
Q

describe the clinical presentation of cows milk allergy

A
  • widespread uricaria (itchy)
  • facial swelling
  • loose stools
  • failure to thrive
  • colic symptoms, GORD
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11
Q

give some severe symptoms a patient with a cows milk allergy may present with

A

wheeze, stridor, abdo pain, diarrhoea/ vomiting, blood/mucus in stools

shock/collapse

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12
Q

how is cows milk allergy managed?

A
  • avoid cows milk
  • if breastfed, ask mother to remove cows milk protein from diet
  • antihistamines if allergic reaction
  • adrenaline in severe reactions

resolves by 5 y/o commonly

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13
Q

describe the presentation post infective lactose intolerance

A

post gastroenteritis watery diarrhoea after reintroducing milk feeds

  • weight loss
  • stools green/ frothy
  • increased frequency
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14
Q

how is post infective lactose intolerance managed and diagnosed?

A

diagnosis- +ve Clinitest

resolves with oral rehydration

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15
Q

describe Toddler’s diarrhoea

A
  • chronic, non-specific diarrhoea
  • commonest cause of persistent loose stools in preschool children
  • presence of mucus and undigested vegetables
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16
Q

how is toddlers diarrhoea managed

A

adequate fat and fibre to slow motility

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17
Q

what is Coeliac Disease?

A

gluten sensitive enteropathy

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18
Q

what is Coeliac disease linked to genetically?

A

human leukocyte antigen (HLA) DQ2

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19
Q

risk factors for Coeliac disease

A

T1DM

autoimmune thyroid disease

Downs

1st degree relatives

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20
Q

describe the GI manifestations of coeliac disease

A
  • malabsorption from 8-24 months of age after the introduction of wheat
  • failure to thrive
  • abdo distention
  • WL
  • buttock wasting
  • abnormal stools (foul smelling) diarrhoea
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21
Q

describe the non-GI manifestations of coeliac disease

A
  • dermatitis herpetiformis- erythematous macules
  • dental enamel defects
  • osteoporosis
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22
Q

how is coeliac disease diagnosed?

A
  • positive serology- IgA tissue transgultaminase TTG antibodies
  • endomysial antibodies
  • small intestinal biopsy to confirm !!

will show mucosal changes (villous atrophy, intraepithelial lymphocytes and crypt hypertrophy)

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23
Q

how is coeliac managed?

A

gluten free diet

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24
Q

what is Crohn’s disease?

A

transmural focal disease most commonly affecting the distal ileum and proximal colon

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25
Q

what are the classical GI manifestations of crohn’s disease?

A
  • abdo pain
  • diarrhoea (bad smelling)
  • weight loss
  • nausea/ vomiting
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26
Q

give some non-intestinal manifestations of Crohns disease

A
  • oral lesions
  • clubbing
  • uveitis
  • arthralgia
  • erythema nodosum
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27
Q

how is Crohn’s diagnosed?

A
  • exclude infection- stool MCS
  • histological findings on biopsy
  • endoscopy
  • abdo barium x ray
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28
Q

how will Crohn’s appear on histology?

A

non-caseating, epitheloid cell granulomata

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29
Q

how will Crohn’s appear on endoscopy?

A
  • small bowel narrowing, fissuring and bowel wall thickened

skip lesions !

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30
Q

how is Crohn’s managed?

A
  • prednisolone
  • immunosuppression- azathioprine/ methotrexate
  • anti-TNF- infliximab
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31
Q

how does ulcerative colitis present clinically?

A

characteristically:

  • rectal bleeding
  • bloody diarrhoea
  • colicky pain
  • weight loss
  • growth failure
  • non-GI manifestations- erythema nodosum and arthritis
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32
Q

how is UC diagnosed?

A
  • exclude infection- stool MCS
  • endoscopy
  • histology
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33
Q

how would UC present on endoscopy?

A
  • loss of goblet cells
  • glandular distortion
  • crypt abscesses
  • mucosal ulcers
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34
Q

how would UC present on histology?

A
  • mucosal inflammation
  • crypt damage
  • ulceration
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35
Q

how can crohn’s and UC be differentiated via a barium swallow X ray?

A

crohns- string sign (string like appearance of severely narrowed intestines)

UC- lead pipe colon

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36
Q

how is UC managed?

A
  • aminosalicylates (5-ASA’s)- sulfasalazine
  • topical steroids
  • azathioprine
  • smoking is protective !
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37
Q

what causes Kwashiorkor disease?

A

due to low intake of protein and essential amino acids

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38
Q

how does kwashiorkor present clinically?

A
  • poor growth
  • diarrhoea
  • apathy
  • anorexia
  • oedema
  • skin/hair depigmentation
  • distended abdomen
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39
Q

how would a patient with kwashiorkor be managed?

A
  • gradually increasing high protein diet + vitamins

- education on diet

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40
Q

what is Marasmus and what is it associated with?

A

lack of calories + discrepancy between height and weight

HIV-associated

41
Q

describe the clinical features of Marasmus

A
  • distended abdo
  • diarrhoea/ constipation
  • infection
  • low albumin
42
Q

how is Marasmus managed?

A

can be managed at home with fortified food

43
Q

what is Intussusception?

A

one segment of the bowel invaginates into another distal to it, leading to obstruct

44
Q

describe the epidemiology of Intussusception

A
  • 6-18 months
  • most common cause of obstruction in children
  • M 3:1 F
45
Q

describe the aetiology of Intussusception

A
  • > 90% non-pathological

- pathological- meckels diverticulum, henoch-schonlein purpura, lymphoma, CF

46
Q

how does Intussusception present clinically?

A
  • sudden onset !
  • paroxysms every 10-20 mins of colicky abdo pain
  • early vomiting- bile stained
  • lethargy
  • sausage-shaped mass in RUQ
  • dances sign
  • ‘red currant jelly’ stools seen late on
47
Q

what is Dances sign?

A
  • seen in Intussusception

absence of bowel sounds in LRQ

48
Q

how is Intussusception diagnosed?

A
  • US- DOUGHNUT OR TARGET SIGN
  • bowel enema- cresent sign
  • abdo- x ray- proximal bowel is dilated and gas-filled
49
Q

how is a patient with Intussusception treated?

A
  • resus
  • reduction with air enema
  • laparotomy
50
Q

when is a laparotomy indicated in a patient initially presenting with Intussusception?

A
  • peritonitis
  • perforation
  • prolonged Hx
  • failed enema
51
Q

when does pyloric stenosis present?

A

3-8 weeks

52
Q

how does pyloric stenosis present?

A
  • projectile vomiting after feeds, no bile
  • constipation
  • dehydration
53
Q

how is pyloric stenosis diagnosed?

A

hypochloraemic, hypokalaemic metabolic alkalosis

  • urine output- dehydrated
54
Q

on examination, what findings would make you suspect pyloric stenosis ?

A
  • clearly visible LUQ peristalsis when feeding

- olive sized pyloric mass

55
Q

how is pyloric stenosis managed?

A
  • correct electrolyte imbalance

- if fails, Ramstedt’s pyloromyotomy

56
Q

when does Mesenteric adenitis typically present, how is it differentiated from appendicitis and how is it managed?

A
  • presents after viral infection
  • differentiated as there is no guarding/ rebound tenderness
  • managed- conservative
57
Q

what is necrotising enterocolitis?

A

inflammatory bowel necrosis

most common GI emergency in neonates

serious intestinal insults to immature gut- toxins, vascular problems etc

58
Q

how does NEC present clinically

A
  • first 2 weeks of life
  • feeding difficulties, vomiting, abdo distension
  • bloody stool
59
Q

how is NEC managed?

A

cefotaxime/ vancomycin

surgery if progressive

60
Q

what is Hirschsprung’s disease and what genes is it associated with?

A

no bowel movements due to missing nerve cells (ganglia) in segment of baby’s colon

MEN 2A/B

61
Q

how does Hirschsprung’s disease present?

A
  • meconium ileus (no bowel movement in 1st 48 hours)
  • abdo distension
  • vomiting
  • constipation
  • megacolon
62
Q

how is Hirschsprung’s disease diagnosed?

A
  • barium x ray

- DIAGNOSTIC- rectal biopsy

63
Q

how is a patient with Hirschsprung’s disease managed?

A
  • bowel washouts/ irrigation- first line

- surgery- bypass affected colon, ileostomy/ colostomy

64
Q

why do neonates have higher bilirubin levels then adults?

A

1) higher concentration of RBCs with short lifespan
2) RBCs breakdown = unconjugated bilirubin
3) unconjugated bilirubin becomes conjugated in liver = liver immaturity = slower conjugation

65
Q

What may be the possible cause of jaundice in neonates at:

<24 hours?

> 14 days?

A

<24hrs = Rhesus haemolytic disease (+ve Coombs test)

> 14 days = Biliary atresia (pale stools)

66
Q

risk factors for jaundice in neonates

A
  • Low BW
  • Prematurity
  • Breast fed babies
  • Maternal diabetes
  • Family Hx
67
Q

how does jaundice present clinically?

A

First seen normally on forehead and face

Neuro signs:
- change in muscle tone, altered crying

  • Pale stools and dark urine
68
Q

what is the name for continued high levels of jaundice?

A

Kernicterus

69
Q

how is jaundice treated?

A

Phototherapy

exchange transfusion

70
Q

what is kernicterus?

A

Acute bilirubin encephalopathy that can cause:

Athetoid movements
Deafness
Low IQ
(brain damage)

prevented by jaundice treatments

71
Q

how does GORD present clinically?

A
  • regurgitation
  • distress after feeds, failure to thrive
  • apnoea
  • pneumonia
  • anaemia
72
Q

how is GORD diagnosed?

A
  • clinical
  • endoscopy
  • ph probe- rarely
73
Q

how is GORD managed?

A
  • avoid over-feeding
  • try thickened feed formula
  • antacid + sodium/ magnesium alginate
  • introduce PPI- ranitidine
74
Q

what should be done after 6-9 months if GORD has not resolved?

A

fundoplication

if failure to thrive, apnoea, bleeding, severe oesophagitis

75
Q

what is Meckel’s Diverticulum?

A

vestigal remnant of the vitellointestinal tract

76
Q

how does Meckel’s diverticulum typically present?

A

-asymptomatic usually

77
Q

give some complications of Meckel’s diverticulum

A
  • haemorrhage (blood in stool)
  • intestinal obstruction
  • diverticulitis
  • perforation
78
Q

how is Meckel’s diverticulum diagnosed?

A
  • always consider in paeds patients with rectal bleeding
  • abdo x ray
  • CT scan
79
Q

how is a paediatric patient with Meckel’s diverticulum managed?

A
  • laparotomy if symptomatic
80
Q

how does a congenital diaphragmatic hernia occur?

A

developmental defect in diaphragm results in herniation of abdo contents into chest

81
Q

what is the main complication of a congenital diaphragmatic hernia?

A

impaired lung development- pulmonary hypoplasia and pulmonary HTN

82
Q

what is gastroschisis?

A

congenital defect, evisceration of abdo contents (opening greater than 5cm)

83
Q

what is exomphalos?

A

herniation of the abdominal contents surrounded in peritoneum

84
Q

how is exomphalos managed?

A

protect herniated viscera to prevent hypothermia and sespsi

closed

85
Q

how does oesophageal atresia present clinically? (prenatally and postnatally)

A

prenatal- polyhydromnias

postnatal- cough, airway obstruction, cyanosis

86
Q

what is biliary atresia?

A

biliary tree occlusion in 3rd week of life

87
Q

how does biliary atresia present?

A

a healthy baby presenting with:

  • jaundice
  • yellow urine
  • pale stools
88
Q

how does acute appendicitis present clinically?

A
  • pain in RIF
  • aggrevated by movement
  • patient will lie still with knees flexed
  • mild fever.
89
Q

symptoms of IBS

A
  • abdominal pain
  • pain relieved on defecation
  • bloating
  • change in bowel habit
  • mucus
90
Q

what is Intussusception?

A

most common cause of intestinal obstruction- one segment of the bowel invaginates onto the other

91
Q

where does intussusception occur?

A

ileocaecal

92
Q

how would a patient with Intussusception typically present?

A
  • sudden onset
  • paroxysms of colicky abdo pain
  • bile stained vomit
93
Q

describe the epidemiology of Intussusception

A

male between 6-18 months

94
Q

symptoms of Malrotation with volvulus

A

bile stained vomiting
circulatory collapse
tender abdo

95
Q

what is Wilsons disease?

A

rare autosomal recessive disorder leading to toxic accumulation of copper in the liver, and eventually in other tissues (brain and eyes)

96
Q

how does Wilson’s disease present clinically?

A
  • Kayser-Fleischer rings

- hepatic problems- hepatitis, cirrhosis,

97
Q

how would you investigate a patient with Wilson’s disease?

A
  • serum copper
  • 24h urinary copper excretion- >100microgram
  • molecular gene testing
98
Q

how is Wilson’s disease treated?

A
  • penicillamine

- liver transplant if end-stage hepatic failure

NP- Phase 3a Medicine (22 decks)

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