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Paeds FOP/TAS > Gastro and Nutrition > Flashcards

Gastro and Nutrition Flashcards

1
Q

Macroscopic and microscopic appearances in UC

A

Macroscopic;
- Continuous inflammation, ulcers, loss of haustra

Microscopic;
- Crypt abscesses, neutrophil infiltration

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2
Q

Macroscopic and microscopic appearances in Crohn’s

A

Macroscopic;
- Cobblestone mucosa, skip lesions, fistula

Microscopic;
- Transmural inflammation, granulomas

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3
Q

Rate of good weight gain in babies

A

15-20g/kg per day

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4
Q

At what point would you expect a baby to regain their birthweight?

A

2 weeks

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5
Q

HLA associations in coeliac disease

A

HLA DQ2 and DQ8

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6
Q

What other conditions are associated with coeliac disease?

A

T1DM
Thyroid disease
AI liver disease
Down syndrome
Turner syndrome

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7
Q

Where is a biopsy taken from to diagnose coeliac disease?

A

Duodenum (affects small bowel mucosa)

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8
Q

Serology tests for coeliac disease

A

IgA and IgA tTG

If IgA deficient will need IgG tTG +/- IgG EMA +/- HLA subtyping (DQ2 + DQ8)

If IgA tTG positive but <10 times upper limit will need biopsy to confirm diagnosis

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9
Q

Extra-GI manifestations of coeliac disease?

A

Dermatitis herpetiformis
Anaemia
Faltering growth
Osteoporosis
Dental enamel defects
Delayed puberty
Recurrent apthous stomatitis
Peripheral neuropathy secondary to B12 deficiency

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10
Q

Most common food allergies

A

Cow’s milk protein
Egg
Peanuts
Tree nuts
Fish
Shellfish
Soya
Wheat

These make up for >90% of allergies

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11
Q

Time span for IgE mediated reaction and non-IgE mediated reactions

A

IgE mediated reactions occur within minutes-2 hours from exposure

Non-IgE mediated reactions occur 2-72 hours following exposure

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12
Q

What % of children will grow out of food allergies (CMPA or egg) by the age of 5?

A

50%

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13
Q

What % of peanut allergies will persist into adulthood?

A

80%

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14
Q

What % of allergies present within the first year of life?

A

80%

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15
Q

What is the most common food allergy in infants <3 months

A

CMPA

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16
Q

What is the gold standard investigation to confirm GORD?

A

pH study

NOTE: GORD is typically a CLINICAL diagnosis and Ix rarely indicated. Should only be done if nil improvement with medical Mx, uncertainty regarding diagnosis or concerns r.e. anatomical abnormality for surgery

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17
Q

What percentage of infants experience GORD?

A

40%

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18
Q

What percentage of infants have resolution of GORD by 1 year?

A

90%

19
Q

Risk factors for GORD in infancy

A

Neurodisability; e.g. Down Sx
Prematurity
Family history of GORD
Previous surgery for oesophageal atresia

20
Q

What condition mimicks GORD?

A

CMPA

21
Q

5 step ladder for managing GORD

A

1) lifestyle; smaller more frequent feeds, keep upright following feeds

2) Thickening agents or alginate therapy (gaviscon)

3) H2 receptor antagonists (ranitidine) or PPI (omeprazole)

4) Prokinetic agents (metoclopramide) - increase gastric emptying

5) Surgery (e.g. Nissen fundoplication)

22
Q

Rule of 2’s for Meckel’s diverticulum

A

Presents <2 yrs of age
2% prevalence in general population
2 inches in length (5cm)
2ft from ileocaecal valve (60cm)

23
Q

What is Meckel’s diverticulum a remnant of?

A

Vitellointestinal duct

24
Q

What specific scan can be done to look for Meckel’s diverticulum?

A

Meckel’s scan; relies on uptake of Tc99m (radioisotope) by ectopic gastric mucosa

25
Q

What specific scan can be done to look for a Meckel’s diverticulum?

A

Meckel’s scan; relies on uptake of TC99m (radioisotope) by ectopic gastric mucosa

26
Q

How may a Meckel’s diverticulum present?

A

Painless PR bleeding (malaena or fresh blood)
Intussusception (abdo pain, bleeding, vomiting)
Bowel obstruction / volvulus
Diverticulitis (abdo pain and diarrhoea)
Incidental finding

27
Q

Which is more common: UC or Crohns?

A

Crohns is twice as common as UC

28
Q

Which type of IBD is smoking considered to be a protective factor?

A

UC

29
Q

Most common age group to get rectal prolapse

A

<4 years of age
Most cases occur within first year of life

30
Q

Causes of rectal prolapse

A

CF (10%)
Idiopathic
Increased abdominal pressure (chronic cough, toilet training, constipation)
Diarrhoeal disorders (malabsorption, infection)
Rectal polyps
Malnutrition
Child abuse (anal sex)

31
Q

Management of rectal prolapse

A

Conservative;
- Dietary advice and laxatives to reduce straining
- Treat underlying causes

Surgery is occasionally required;
- Recurrent prolapses
- Resistant prolapse
- Ulceration
- Significant pain (usually painless)

32
Q

Typical dystonic posturing seen in Sandifer syndrome

A
  • Sudden deviation of the head and neck to one side and legs to the other side stretched out
  • Back arches posteriorly
  • Hyperextension of the spine
  • Hyper-extendable hips
  • Elbows flexed and held posteriorly
33
Q

Cholestasis, heart murmur, butterfly vertebra

A

Alagille Sx

34
Q

Causes of conjugated and unconjugated jaundice

A

Unconjugated = pre-hepatic

Conjugated = hepatic or post hepatic

35
Q

Which enzyme conjugates bilirubin?

A

Bilirubin uridine diphosphate glucuronosyltransferase (UGT)

Conjugates bilirubin with glucuronic acid to make it water soluble

36
Q

Most common causes of a conjugated jaundice

A

Idiopathic neonatal hepatitis

Viral hepatitis

Extrahepatic biliary atresia

Intrahepatic cholestasis syndrome (Alagille, alpha 1 antitrypsin)

37
Q

Causes of Unconjugated jaundice

A

Pre-hepatic!

Haemolysis:
- Thalassaemia
- Sickle cell
- ABO/rhesus incompatibility
- HUS
- Spherocytosis
- Polycythaemia

Physiological / breast milk

Infection

Inherited disorders;
- Crigler-Najjar (sick baby)
- Gilbert (asymptomatic)

38
Q

Causes of Conjugated jaundice

A

Hepatic or post-hepatic!

  • Idiopathic neonatal hepatitis
  • Viral hepatitis (Hep A/B, CMV, EBV, enterovirus)
  • Extrahepatic biliary atresia
  • Intrahepatic cholestasis syndrome (Alagille, alpha 1 antitrypsin)
  • Bacterial sepsis
  • Parasitic (malaria)
  • Metabolic disorders (glycogen storage disease, Niemann-Pick, mitochondrial disorders)
  • Biliary tree disorders (Caroli Sx)
  • Hypothyroidism
  • Cystic Fibrosis
39
Q

At what blood bili level does Jaundice become visible?

A

80-100

40
Q

Management of cholestatic liver disease

A

Ursodeoxycholic acid

Vitamins ADEK (fat soluble)

41
Q

Sequelae of kernicterus

A

Athetoid cerebral palsy
High frequency hearing loss
Paralysis of upward gaze
Dental dysplasia
Learning disability

42
Q

Risk factors for developing kernicterus

A

Serum bili >340 in a neonate >37 wks gestational age

Rapidly rising bili >8.5 per hr

Clinical features of bilirubin encephalopathy

43
Q

Pathophysiology of kernicterus

A

High levels of unbound, lipid-soluble, conjugated bilirubin crossing the blood-brain barrier

Paeds FOP/TAS (12 decks)

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